Anti-metastatic https://greenmedinfo.com/category/keywords/Anti-metastatic en A comprehensive review on anticancer mechanisms of crocin. https://greenmedinfo.com/article/comprehensive-review-anticancer-mechanisms-crocin n/a PMID:  J Pharm Pharmacol. 2017 Jul 3. Epub 2017 Jul 3. PMID: 28675431 Abstract Title:  A comprehensive review on anticancer mechanisms of the main carotenoid of saffron, crocin. Abstract:  OBJECTIVES: Crocin is derived from dried stigmas of Crocus sativus L. (saffron). It has long been used to prevent and treat various diseases. Although crocin is suggested as one of the most effective cancer therapeutic constituents of saffron stigma, its exact molecular mechanisms are not fully understood. In this study, we reviewed anticancer effects of crocin and its underlying molecular mechanisms. KEY FINDINGS: While several mechanisms may account for the antitumour activity of crocin, alteration of expression/activity of the genes and also epigenetic changes may be considered as necessary phenomena. These alternations may lead to inhibition of cancer cells' proliferation or/and induction of apoptosis through various mechanism including inhibition of synthesis of DNA and RNA, interaction with cellular topoisomerase, suppression of the telomerase activity and active STAT3, and targeting of microtubules. Moreover, this carotenoid could reverse the epithelial-mesenchymal transition and inhibit metastasis. CONCLUSIONS: Knowing molecular mechanisms of antitumoral agents could guide us to choose the best chemotherapeutic compound especially for targeted therapy and also provide insights about possible side effects. https://greenmedinfo.com/article/comprehensive-review-anticancer-mechanisms-crocin#comments Cancers: All Crocin Anti-metastatic Antiproliferative Apoptotic Chemotherapeutic Telomerase Inhibitor Anti-metastatic Antiproliferative Apoptotic Cancers: All Chemotherapeutic Crocin Telomerase Inhibitor Review Fri, 14 Jul 2017 01:19:14 +0000 greenmedinfo 150415 at https://greenmedinfo.com A polysaccharide from Punica granatum has an inhibitory effect on metastasis. https://greenmedinfo.com/article/polysaccharide-punica-granatum-has-inhibitory-effect-metastasis n/a PMID:  Int J Biol Macromol. 2017 May 25. Epub 2017 May 25. PMID: 28552725 Abstract Title:  The inhibitory effect of anti- tumor polysaccharide from Punica granatum on metastasis. Abstract:  Galactomannan (PSP001) isolated from the fruit rind of Punica granatum was demonstrated as an excellent antioxidant, immunomodulatory and anticancer agent both in vitro and in vivo models. Since the most lethal and debilitating attribute of cancer cells is their ability to evolve to a state of malignancy, with key features like increased angiogenesis, invasion, migration, colony formation, and metastasis, the present study focused on evaluating the effects of the galactomannan on tumor and malignancy. PSP001 effectively reduced the neovascularization in chick embryos highlighting its potential as an angiogenic inhibitor. Furthermore, the invasion, migration and clonogenic capacity of human and murine cancer cells were dramatically inhibited by PSP001. Evaluation of the molecular mechanism of its unique potential revealed the down regulation of key players including VEGF, MMP-2, and MMP-9 with marked elevation of TIMP-1 and TIMP-2. The anti-metastatic potential of PSP001 tested in pulmonary metastasis C57BL/6 mice model deciphered the combinatorial administration with vincristine deliberated better survival rates and decreased metastatic index. The angiogenic inhibition potential of PSP001 was further proved with peritoneal angiogenesis assay in BALB/c mice ascitic tumor model. The outcomes of the current investigation highlight the mode of action of antitumor galactomannan in the reduction of tumor malignancy. https://greenmedinfo.com/article/polysaccharide-punica-granatum-has-inhibitory-effect-metastasis#comments Cancer Metastasis Lung Cancer: Metastatic Pomegranate Anti-metastatic Anti-metastatic Cancer Metastasis Lung Cancer: Metastatic pomegranate Animal Study Thu, 01 Jun 2017 23:17:36 +0000 greenmedinfo 148588 at https://greenmedinfo.com A review of the multiple targets and signalling pathways of ginsenosides in cancers. https://greenmedinfo.com/article/review-multiple-targets-and-signalling-pathways-ginsenosides-cancers n/a PMID:  Evid Based Complement Alternat Med. 2016 ;2016:5738694. Epub 2016 Jun 30. PMID: 27446225 Abstract Title:  Anticancer Activities of Protopanaxadiol- and Protopanaxatriol-Type Ginsenosides and Their Metabolites. Abstract:  Recently, most anticancer drugs are derived from natural resources such as marine, microbial, and botanical sources, but the low success rates of chemotherapies and the development of multidrug resistance emphasize the importance of discovering new compounds that are both safe and effective against cancer. Ginseng types, including Asian ginseng, American ginseng, and notoginseng, have been used traditionally to treat various diseases, due to their immunomodulatory, neuroprotective, antioxidative, and antitumor activities. Accumulating reports have shown that ginsenosides, the major active component of ginseng, were helpful for tumor treatment. 20(S)-Protopanaxadiol (PDS) and 20(S)-protopanaxatriol saponins (PTS) are two characteristic types of triterpenoid saponins in ginsenosides. PTS holds capacity to interfere with crucial metabolism, while PDS could affect cell cycle distribution and prodeath signaling. This review aims at providing an overview of PTS and PDS, as well as their metabolites, regarding their different anticancer effects with the proposal that these compounds might be potent additions to the current chemotherapeutic strategy against cancer. https://greenmedinfo.com/article/review-multiple-targets-and-signalling-pathways-ginsenosides-cancers#comments Cancers: All Ginsenosides Anti-Inflammatory Agents Anti-metastatic Antiproliferative Cell cycle arrest Anti-Inflammatory Agents Anti-metastatic Antiproliferative Cancers: All Cell cycle arrest Ginsenosides Review Wed, 28 Dec 2016 00:10:14 +0000 greenmedinfo 141075 at https://greenmedinfo.com An extract of Litchi seed has potential for development into a safe and potent alternative therapy for prostate cancer patients. https://greenmedinfo.com/article/extract-litchi-seed-has-potential-development-safe-and-potent-alternative-ther n/a PMID:  Sci Rep. 2017 Jan 30 ;7:41656. Epub 2017 Jan 30. PMID: 28134352 Abstract Title:  Litchi seed extracts diminish prostate cancer progression via induction of apoptosis and attenuation of EMT through Akt/GSK-3β signaling. Abstract:  Litchi (Litchi chinensisSonnnerat, Sapindaceae), known as Chinese Cherry, is a subtropical fruit tree originating from southern China. Litchi seed extracts have diverse pharmacological effects, including anticancer. However, its anticancer effects and mechanisms on prostate cancer have not been determined. In this study, we used n-butyl alcohol extract of Litchi seed (NLS) to treat prostate cancer PC3, DU145, RM1 and C4-2B cells. NLS induced a significant decrease in cell viability and clonogenic growth in a dose-dependent manner. NLS induced cell apoptosis and cell cycle G1/S phase arrest by inactivating Akt signaling pathway, which were associated with activation of mitochondrial caspase-dependent apoptotic cascades, up-regulation of cyclin-dependent kinase (CDK) inhibitors p21 and p27, and inhibition of correlated cyclin/CDK network. In addition, NLS treatment significantly decreased cell migration and invasion via phenotypic inversion of EMT, correlated with increased expression of E-cadherin andβ-catenin, and decreased expression of vimentin and snail, which is partially attributed to inhibiting Akt/GSK-3β signaling pathway. Finally, PC3 xenograft nude mice treated with NLS in vivo showed a significant decrease in tumor size without toxicity. These findings suggest that NLS has potentialfor development into a safe and potent alternative therapy for prostate cancer patients. https://greenmedinfo.com/article/extract-litchi-seed-has-potential-development-safe-and-potent-alternative-ther#comments Litchi Prostate Cancer Anti-metastatic Apoptotic Cell cycle arrest P21 Activation Anti-metastatic Apoptotic Cell cycle arrest Litchi P21 Activation Plant Extracts prostate cancer Animal Study In Vitro Study Tue, 31 Jan 2017 16:42:51 +0000 greenmedinfo 142799 at https://greenmedinfo.com Curcumin exerts its tumor suppressive function via inhibition of NEDD4 oncoprotein in glioma cancer cells. https://greenmedinfo.com/article/curcumin-exerts-its-tumor-suppressive-function-inhibition-nedd4-oncoprotein-gl n/a PMID:  Int J Oncol. 2017 Jun 8. Epub 2017 Jun 8. PMID: 28627598 Abstract Title:  Curcumin exerts its tumor suppressive function via inhibition of NEDD4 oncoprotein in glioma cancer cells. Abstract:  Glioblastoma is the most common brain cancer in adults. It represents one of the top ten malignant tumors with an average survival time of nine months despite treatments with surgery, radiotherapy and chemotherapy. Curcumin is a phytochemical turmeric isolated from root of the Curcuma longa plant. Accumulating evidence have proved that curcumin targets numerous cancer signaling pathways. The E3 ubiquitin ligase NEDD4, neural precursor cell expressed developmentally downregulated protein 4, is frequently overexpressed in various cancers. However, whether curcumin regulates NEDD4 expression has not been described in human cancers. Therefore, in this study, we explored the roles of NEDD4 in glioma cell proliferation, apoptosis and mobility. We further investigated whether curcumin exerts its antitumor activities via suppressing NEDD4 expression. We found that curcumin reduced the expression of NEDD4 and Notch1 and pAKT, leading to glioma cell growth inhibition, apoptosis, and suppression of migration and invasion. Moreover, deletion of NEDD4 expression enhanced the sensitivity of glioma cells to curcumin treatment. Thus, inactivation of NEDD4 by curcumin could be a promising approach for therapeutic intervention. https://greenmedinfo.com/article/curcumin-exerts-its-tumor-suppressive-function-inhibition-nedd4-oncoprotein-gl#comments Curcumin Glioma Anti-metastatic Antiproliferative Apoptotic Anti-metastatic Antiproliferative Apoptotic CURCUMIN Glioma In Vitro Study Sat, 24 Jun 2017 01:52:02 +0000 greenmedinfo 149576 at https://greenmedinfo.com Delta-tocotrienol inhibits pancreatic cancer stem-like cells and prevents pancreatic cancer metastasis. https://greenmedinfo.com/article/delta-tocotrienol-inhibits-pancreatic-cancer-stem-cells-and-prevents-pancreati n/a PMID:  Oncotarget. 2017 May 9 ;8(19):31554-31567. PMID: 28404939 Abstract Title:  δ-Tocotrienol, a natural form of vitamin E, inhibits pancreatic cancer stem-like cells and prevents pancreatic cancer metastasis. Abstract:  The growth, metastasis, and chemotherapy resistance of pancreatic ductal adenocarcinoma (PDAC) is characterized by the activation and growth of tumor-initiating cells in distant organs that have stem-like properties. Thus, inhibiting growth of these cells may prevent PDAC growth and metastases. We have demonstrated thatδ-tocotrienol, a natural form of vitamin E (VEDT), is bioactive against cancer, delays progression, and prevents metastases in transgenic mouse models of PDAC. In this report, we provide the first evidence that VEDT selectively inhibits PDAC stem-like cells. VEDT inhibited the viability, survival,self-renewal, and expression of Oct4 and Sox2 transcription factors in 3 models of PDAC stem-like cells. In addition, VEDT inhibited the migration, invasion, and several biomarkers of epithelial-to-mesenchymal transition and angiogenesis in PDAC cells and tumors. These processes are critical for tumor metastases. Furthermore, in the L3.6pl orthotopic model of PDAC metastases, VEDT significantly inhibited growth and metastases of these cells. Finally, in an orthotopic xenograft model of human PDAC stem-like cells, we showed that VEDT significantly retarded the growth and metastases of gemcitabine-resistant PDAC human stem-like cells. Because VEDT has been shown to be safe and to reach bioactive levels in humans, this work supports investigating VEDT for chemoprevention of PDAC metastases. https://greenmedinfo.com/article/delta-tocotrienol-inhibits-pancreatic-cancer-stem-cells-and-prevents-pancreati#comments Pancreatic Cancer Tocotrienol: Delta Vitamin E Anti-metastatic Antiproliferative Chemopreventive Anti-metastatic Antiproliferative Cancer Stem Cells Chemopreventive Pancreatic Cancer Tocotrienol: Delta VITAMIN E In Vitro Study Wed, 21 Jun 2017 02:37:09 +0000 greenmedinfo 149382 at https://greenmedinfo.com Garcinone E exerts anticancer activities by inducing apoptosis and suppressing migration and invasion in ovarian cancer cells. https://greenmedinfo.com/article/garcinone-e-exerts-anticancer-activities-inducing-apoptosis-and-suppressing-mi n/a PMID:  Sci Rep. 2017 Sep 6 ;7(1):10718. Epub 2017 Sep 6. PMID: 28878295 Abstract Title:  Garcinone E induces apoptosis and inhibits migration and invasion in ovarian cancer cells. Abstract:  Ovarian cancer remains the most lethal gynecological malignant tumor. In this study, 24 xanthones were isolated and identified from the pericarps of mangosteen (Garcinia mangostana), and their anti-proliferative activities were tested in ovarian cancer cells. Garcinone E (GE) was found to exhibit excellent anti-proliferative effects among the tested xanthones. It significantly inhibited the proliferation in HEY, A2780, and A2780/Taxol cells as evidenced by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay, lactate dehydrogenase (LDH) release assay, Hoechst 33342 staining, annexin V/PI staining, and JC-1 staining. It induced endoplasmic reticulum (ER) stress and activated the protective inositol-requiring kinase (IRE)-1α pathway. Knocking down IRE-1α further activated the caspase cascade and caused an increase in cell death. Moreover, GE eliminated the migratory ability of HEY cells by reducing the expression of RhoA and Rac. It also blocked the invasion, which might be related to downregulation of matrix metalloproteinases (MMPs), i.e., MMP-9 and MMP-2, and upregulation of tissue inhibitors of metalloproteinase (TIMP) -1 and TIMP-2. In summary, GE exerts anticancer activities by inducing apoptosis and suppressing migration and invasion in ovarian cancer cells, which indicates its therapeutic potential forovarian cancer. https://greenmedinfo.com/article/garcinone-e-exerts-anticancer-activities-inducing-apoptosis-and-suppressing-mi#comments Garcinia Mangostana Ovarian Cancer Anti-metastatic Apoptotic Matrix metalloproteinase-2 (MMP-2) inhibitor Matrix metalloproteinase-9 (MMP-9) inhibitor Anti-metastatic Apoptotic Garcinia Mangostana ovarian cancer In Vitro Study Thu, 11 Jan 2018 16:13:53 +0000 greenmedinfo 158311 at https://greenmedinfo.com Genistein inhibits the growth and regulates the migration and invasion abilities of melanoma. https://greenmedinfo.com/article/genistein-inhibits-growth-and-regulates-migration-and-invasion-abilities-melan n/a PMID:  Oncotarget. 2017 Mar 28 ;8(13):21674-21691. PMID: 28423510 Abstract Title:  Genistein inhibits the growth and regulates the migration and invasion abilities of melanoma cells via the FAK/paxillin and MAPK pathways. Abstract:  Genistein is one of the main components of soy-based foods, which are widely known for their many benefits, including anti-cancer, anti-inflammatory, and antioxidant effects. In this study, we investigated the anti-metastasis effects of genistein on B16F10 melanoma cells. Our results showed that genistein strongly inhibited B16F10 cell proliferation and induced apoptosis in time- and concentration-dependent manners. Genistein altered the morphology of B16F10 cells to an elongated shape with slim pseudopodia-like protrusions. Moreover, genistein inhibited the invasion and migration abilities of B16F10 cells in a dose-dependent manner. On one hand, a high concentration of genistein (100μM) significantly inhibited cell adhesion and migration, as shown by wound healing assays and transwell-migration and invasion assays. Furthermore, the expression levels of p-FAK, p-paxillin, tensin-2, vinculin, and α-actinin were decreased by genistein. As a result, genistein is believed to strongly downregulate the migration and invasion abilities of B16F10 cells via the FAK/paxillin pathway. Moreover, p-p38, p-ERK, and p-JNK levels were also dramatically decreased by treatment with genistein. Finally, genistein significantly decreased the gene expression of FAK, paxillin, vimentin, and epithelial-to-mesenchymal transition-related transcription factor Snail, as shown by real-time PCR (qPCR) analysis. On the other hand, a lower concentration of genistein (12.5 μM) significantly promoted both invasion and migration by activating the FAK/paxillin and MAPK signaling cascades. Taken together, this study showed for the first time that genistein exerts dual functional effects on melanoma cells. Our findings suggest that genistein regulates the FAK/paxillin and MAPK signaling pathways in a highly concentration-dependent manner. Patients with melanoma should therefore be cautious of consuming soy-based foods in their diets. https://greenmedinfo.com/article/genistein-inhibits-growth-and-regulates-migration-and-invasion-abilities-melan#comments Genistein Melanoma Anti-metastatic Anti-metastatic Genistein melanoma In Vitro Study Tue, 08 Aug 2017 01:23:21 +0000 greenmedinfo 151295 at https://greenmedinfo.com Ginsenoside Rb1 may be a potential therapeutic candidate for the treatment of ovarian cancer. https://greenmedinfo.com/article/ginsenoside-rb1-may-be-potential-therapeutic-candidate-treatment-ovarian-cance n/a PMID:  Exp Ther Med. 2017 Oct ;14(4):2895-2902. Epub 2017 Aug 4. PMID: 28928801 Abstract Title:  Ginsenoside Rb1 inhibits hypoxia-induced epithelial-mesenchymal transition in ovarian cancer cells by regulating microRNA-25. Abstract:  Metastasis frequently occurs in advanced ovarian cancer, which not only leads to substantial mortality but also becomes a major challenge to effective treatment. Epithelial-mesenchymal transition (EMT) is a key mechanism facilitating cancer metastasis. Targeting the EMT process with more efficacious and less toxic agents to prevent metastasis is of significant therapeutic value for ovarian cancer treatment. The anti-EMT function and mechanism of ginsenoside Rb1, a monomer composition extracted from the traditional Chinese herbor, was investigated in the present study. Western blotting demonstrated that treatment with ginsenoside Rb1 antagonized hypoxia-induced E-cadherin downregulation and vimentin upregulation in SKOV3 and 3AO human ovarian cancer cells. Wound healing assays andmigration assays indicated that ginsenoside Rb1 weakened hypoxia-enhanced cell migration ability. Furthermore, it was demonstrated that microRNA (miR)-25 is upregulated by hypoxia in ovarian cancer cells, which was attenuated by ginsenoside Rb1 treatment. Additionally, forced expression of miR-25 in ovarian cancer cells was identified to not only trigger EMT, but also block the suppressive effects of ginsenoside Rb1 on hypoxia-induced EMT by negatively targeting the E-cadherin transactivator, EP300. In conclusion, ginsenoside Rb1 may reverse hypoxia-induced EMT by abrogating the suppression of miR-25 on EP300 and E-cadherin, which suggests that ginsenoside Rb1 may be a potential therapeutic candidate for the treatment of ovarian cancer. https://greenmedinfo.com/article/ginsenoside-rb1-may-be-potential-therapeutic-candidate-treatment-ovarian-cance#comments Ginsenosides Ovarian Cancer Anti-metastatic Anti-metastatic Ginsenosides ovarian cancer In Vitro Study Fri, 02 Mar 2018 08:52:57 +0000 greenmedinfo 160628 at https://greenmedinfo.com Hesperidin inhibited the migratory and invasive capabilities of A549 human non-small cell lung cancer cells. https://greenmedinfo.com/article/hesperidin-inhibited-migratory-and-invasive-capabilities-a549-human-non-small- n/a PMID:  Life Sci. 2018 Mar 28. Epub 2018 Mar 28. PMID: 29604270 Abstract Title:  Hesperidin suppresses the migration and invasion of non-small cell lung cancer cells by inhibiting the SDF-1/CXCR-4 pathway. Abstract:  OBJECTIVE: The present study aimed to investigate the ability of hesperidin to suppress the migration and invasion of A549 cells, and to investigate the role of the SDF-1/CXCR-4 cascade in this suppression. METHODS: We performed a Transwell migration assay to measure the migratory capability of A549 cells treated with 0.5% DMSO, SDF-1α, AMD3100 or hesperidin. The SDF-1 level in the culture medium was determined by an enzyme-linked immunosorbent assay (ELISA) to detect whether different concentrations of hesperidin affected SDF-1 secretion. A wound-healing assay was performed to determine the effects of different concentrationsof hesperidin on the migration inhibition of A549, H460 and H1975 cells. Additionally, the effect of various hesperidin concentrations on the rate of A549 cell invasion and migration was examined with and without Matrigel in Transwell assays, respectively. Western blot analysis was used to evaluatethe protein levels of CXCR-4, MMP-9, CK-19, Vimentin, p65, p-p65, p-IκB, IκB, p-Akt and Akt. RT-qPCR was used to detect the mRNA levels of CXCR-4, MMP-9, CK-19, Vimentin, p65, IκB, SDF-1 and Akt. RESULTS: The Transwell migration assay indicated that SDF-1α promoted A549 cell migration, while AMD3100 and hesperidin significantly inhibited the migratory capability. The wound-healing assay demonstrated that hesperidin treatment significantly reduced the rate of wound closure compared with the control group in a dose-dependent manner. Similarly, the migration and invasive abilities of A549 cells, H460 and H1975 cells treated with hesperidin were significantly decreased compared with the control group. The ELISA data suggested that hesperidin attenuated the secretion of SDF-1 from A549 cells in a dose-dependent manner. Furthermore, western blot analysis indicated that SDF-1α treatment significantly increased the levels of CXCR-4, p-p65, p-IκB and p-Akt in A549 cells. In contrast, AMD3100 or hesperidin reversed the effect induced by SDF-1α through decreasing the expression of CXCR-4. Subsequent RT-qPCR and western blot analyses also confirmed that hesperidin had a significant effect on the expression of EMT-related proteins, including MMP-9, CK-19 and Vimentin, in A549 cells. CONCLUSION: In summary, we demonstrated that hesperidin inhibited the migratory and invasive capabilities of A549 human non-small cell lung cancer cells by the mediation of the SDF-1/CXCR-4 signaling cascade, thus providing the foundation for the development of hesperidin as a safer and more effective anticancer drug for non-small cell lung cancer. https://greenmedinfo.com/article/hesperidin-inhibited-migratory-and-invasive-capabilities-a549-human-non-small-#comments Hesperidin Non-Small-Cell Lung Carcinoma Anti-metastatic Matrix metalloproteinase-9 (MMP-9) inhibitor Anti-metastatic Hesperidin Matrix metalloproteinase-9 (MMP-9) inhibitor Non-Small-Cell Lung Carcinoma In Vitro Study Sat, 07 Apr 2018 02:45:56 +0000 greenmedinfo 162319 at https://greenmedinfo.com Increase in motility and invasiveness of MCF7 cancer cells induced by nicotine is abolished by melatonin. https://greenmedinfo.com/article/increase-motility-and-invasiveness-mcf7-cancer-cells-induced-nicotine-abolishe n/a PMID:  J Pineal Res. 2018 Jan 16. Epub 2018 Jan 16. PMID: 29338098 Abstract Title:  Increase in motility and invasiveness of MCF7 cancer cells induced by nicotine is abolished by melatonin through inhibition of ERK phosphorylation. Abstract:  Through activation of the ERK pathway nicotine, in both normal MCF-10A and low malignant breast cancer cells (MCF7), promotes increased motility and invasiveness. Melatonin antagonizes both these effects by inhibiting almost completely ERK phosphorylation. As melatonin has no effect on not-stimulated cells, it is likely that melatonin can counteract ERK-activation only downstream of nicotine-induced activation. This finding suggests that melatonin hampers ERK phosphorylation presumably by targeting a still unknown intermediate factor that connects nicotine stimulation to ERK phosphorylation. Furthermore, downstream of ERK activation, melatonin significantly reduces Fascin and Calpain activation while restoring normal Vinculin levels. Melatonin also counteracts nicotine effects by reshaping the overall cytoskeleton architecture and abolishing invasive membrane protrusion. In addition, melatonin decreases nicotine-dependent ROCK1/ROCK2 activation, thus further inhibiting cell contractility and motility. Melatonin actions are most likely attributable to ERK inhibition, although melatonin could display other ERK-independent effects, namely through a direct modulation of additional molecular and structural factors, including Coronin, Cofilin and cytoskeleton components. This article is protected by copyright. All rights reserved. https://greenmedinfo.com/article/increase-motility-and-invasiveness-mcf7-cancer-cells-induced-nicotine-abolishe#comments Breast Cancer Melatonin Nicotine/Tobacco Toxicity Anti-metastatic Anti-metastatic Breast Cancer melatonin Nicotine/Tobacco Toxicity In Vitro Study Fri, 19 Jan 2018 17:03:26 +0000 greenmedinfo 158590 at https://greenmedinfo.com Puerarin can inhibit the adhesion, invasion and migration of oophoroma HO-8910 cells. https://greenmedinfo.com/article/puerarin-can-inhibit-adhesion-invasion-and-migration-oophoroma-ho-8910-cells n/a PMID:  Zhongguo Zhong Xi Yi Jie He Za Zhi. 2009 Jul ;29(7):632-5. PMID: 19852298 Abstract Title:  [Inhibitory effects of puerarin on invasion and metastasis of oophoroma cells HO-8910]. Abstract:  OBJECTIVE: To investigate the inhibitory effect of puerarin on invasive and metastatic abilities of tumor cells, and its possible mechanism through observing its impacts on the migratory, adhesive and invasive capacities of human oophoroma cells HO-8910 to the artificial recombined basement membrane. METHODS: Expression of estrogen receptor (ER) in HO-8910 cells was detected using PCR assay. Effects of puerarin on HO-8910 proliferation was detected with MTT assay; on its adhesion potential was tested with cell-matrigel adhesion assay, and on invasive and migratory capacities were measured with Transwell matrigel invasion assay and Transwell motility assay respectively. RESULTS: ER was positively expressed in HO-8910 cells. After being treated with 20 micromol/L puerarin for 12 h, the adhesive test showed that OD value in the tested group was significantly lower than that in the control (P<0.01), the inhibiting rate reached 50.63%; and the Transwell assay showed a significant lowering of penetrated cells (P<0.01), the inhibition rate for invasion was 38.59% and that for motility migration 40.63%. The number of penetrated cells was lower in the group intervened with combination of Puerarin and estrogen than in the group intervened with estrogen alone, 33.40 +/- 3.30 vs 48.05 +/- 3. 56 for invasion and 35.35 +/- 3.03 vs 52.45 +/- 1.04 for motility (all P<0.01). CONCLUSION: Puerarin can inhibit the adhesion, invasion and migration of HO-8910 cells, plays an antagonist effect against the stimulation of estrogen on the malignant behavior of tumor cells. https://greenmedinfo.com/article/puerarin-can-inhibit-adhesion-invasion-and-migration-oophoroma-ho-8910-cells#comments Cancer Metastasis Ovarian Cancer Puerarin Anti-metastatic Anti-metastatic Cancer Metastasis ovarian cancer Puerarin In Vitro Study Wed, 06 Jun 2018 23:54:03 +0000 greenmedinfo 165390 at https://greenmedinfo.com Resveratrol prevents endothelial cells injury in high-dose interleukin-2 therapy against melanoma. https://greenmedinfo.com/article/resveratrol-prevents-endothelial-cells-injury-high-dose-interleukin-2-therapy- n/a PMID:  PLoS One. 2012 ;7(4):e35650. Epub 2012 Apr 20. PMID: 22532866 Abstract Title:  Resveratrol prevents endothelial cells injury in high-dose interleukin-2 therapy against melanoma. Abstract:  Immunotherapy with high-dose interleukin-2 (HDIL-2) is an effective treatment for patients with metastatic melanoma and renal cell carcinoma. However, it is accompanied by severe toxicity involving endothelial cell injury and induction of vascular leak syndrome (VLS). In this study, we found that resveratrol, a plant polyphenol with anti-inflammatory and anti-cancer properties, was able to prevent the endothelial cell injury and inhibit the development of VLS while improving the efficacy of HDIL-2 therapy in the killing of metastasized melanoma. Specifically, C57BL/6 mice were injected with B16F10 cells followed by resveratrol by gavage the next day and continued treatment with resveratrol once a day. On day 9, mice received HDIL-2. On day 12, mice were evaluated for VLS and tumor metastasis. We found that resveratrol significantly inhibited the development of VLS in lung and liver by protecting endothelial cell integrity and preventing endothelial cells from undergoing apoptosis. The metastasis and growth of the tumor in lung were significantly inhibited by HDIL-2 and HDIL-2 + resveratrol treatment. Notably, HDIL-2 + resveratrol co-treatment was more effective in inhibiting tumor metastasis and growth than HDIL-2 treatment alone. We also analyzed the immune status of Gr-1(+)CD11b(+) myeloid-derived suppressor cells (MDSC) and FoxP3(+)CD4(+) regulatory T cells (Treg). We found that resveratrol induced expansion and suppressive function of MDSC which inhibited the development of VLS after adoptive transfer. However, resveratrol suppressed the HDIL-2-induced expansion of Treg cells. We also found that resveratrol enhanced the susceptibility of melanoma to the cytotoxicity of IL-2-activated killer cells, and induced the expression of the tumor suppressor gene FoxO1. Our results suggested the potential use of resveratrol in HDIL-2 treatment against melanoma. We also demonstrated, for the first time, that MDSC is the dominant suppressor cell than regulatory T cell in the development of VLS. https://greenmedinfo.com/article/resveratrol-prevents-endothelial-cells-injury-high-dose-interleukin-2-therapy-#comments Lung Cancer Melanoma Resveratrol Anti-metastatic Chemoprotective Agents Chemosensitizer Anti-metastatic Chemoprotective Agents Chemosensitizer lung cancer melanoma RESVERATROL In Vitro Study Thu, 20 Jul 2017 00:40:59 +0000 greenmedinfo 150717 at https://greenmedinfo.com Shikonin and temozolomide may constitute a powerful new tool for Glioblastoma treatment by reducing therapy resistance and tumor recurrence. https://greenmedinfo.com/article/shikonin-and-temozolomide-may-constitute-powerful-new-tool-glioblastoma-treatm n/a PMID:  Cell Oncol (Dordr). 2017 Apr 11. Epub 2017 Apr 11. PMID: 28401486 Abstract Title:  Dual treatment with shikonin and temozolomide reduces glioblastoma tumor growth, migration and glial-to-mesenchymal transition. Abstract:  PURPOSE: Glioblastomas (GBM) comprise 17% of all primary brain tumors. These tumors are extremely aggressive due to their infiltrative capacity and chemoresistance, with glial-to-mesenchymal transition (GMT) proteins playing a prominent role in tumor invasion. One compound that has recently been used to reduce the expression of these proteins is shikonin (SHK), a naphthoquinone with anti-tumor properties. Temozolomide (TMZ), the most commonly used chemotherapeutic agent in GBM treatment, has so far not been studied in combination with SHK. Here, we investigated the combined effects of these two drugs on the proliferation and motility of GBM-derived cells. METHODS: The cytotoxic and proliferative effects of SHK and TMZ on human GBM-derived cells were tested using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT), Ki67 staining and BrdU incorporation assays. The migration capacities of these cells were evaluated using a scratch wound assay. The expression levels ofβ3 integrin, metalloproteinases (MMPs) and GMT-associated proteins were determined by Western blotting and immunocytochemistry. RESULTS: We found that GBM-derived cells treated with a combination of SHK and TMZ showed decreases in their proliferation and migration capacities. These decreases were followed by the suppression of GMT through a reduction ofβ3 integrin, MMP-2, MMP-9, Slug and vimentin expression via inactivation of PI3K/AKT signaling. CONCLUSION: From our results we conclude that dual treatment with SHK and TMZ may constitute a powerful new tool for GBM treatment by reducing therapy resistance and tumor recurrence. https://greenmedinfo.com/article/shikonin-and-temozolomide-may-constitute-powerful-new-tool-glioblastoma-treatm#comments Glioblastoma Shikonin Anti-metastatic Antiproliferative Matrix metalloproteinase-2 (MMP-2) inhibitor Matrix metalloproteinase-9 (MMP-9) inhibitor Anti-metastatic Antiproliferative Chemotherapeutic Synergy: Temozolomide Glioblastoma Shikonin Human In Vitro Wed, 03 May 2017 15:01:18 +0000 greenmedinfo 147157 at https://greenmedinfo.com The cytotoxic effects of the Stanley and Fortress onion varieties were strongest among the selected cultivars. https://greenmedinfo.com/article/cytotoxic-effects-stanley-and-fortress-onion-varieties-were-strongest-among-se n/a PMID:  Food Res Int. 2017 Jun ;96:12-18. Epub 2017 Mar 11. PMID: 28528091 Abstract Title:  Antiproliferative activity of Ontario grown onions against colorectal adenocarcinoma cells. Abstract:  Cancer is the leading cause of mortality in Canada and other industrialized nations; the development of new/improved cancer therapies is desperately needed and continues to be a major focus of cancer research. Flavonoids, which are found in high levels in onions, have been shown to exert antiproliferative and potentially anti-cancer activities. To test their therapeutic potential, we assessed the antiproliferative, cytotoxic, apoptosis-inducing, and anti-migratory activities of five onion varieties grown in Ontario against human adenocarcinoma (Caco-2) cells. The properties of onion extracts were compared to pure extracts of flavonoids known to exhibit antiproliferative effects (quercetin, myricetin, and kaempferol). We compared more than one variety of onion, as agronomic and genetic factors influence the composition, as well as the quality of phytochemicals (e.g. flavonoids) in plant cultivars. We found that all onion varieties exhibited antiproliferative activity similar to purified flavonoids. The cytotoxic effects of the Stanley and Fortress onion varieties were strongest among the selected cultivars, as determined via lactate dehydrogenase (LDH) assays, while Safrane extracts showed the weakest activity. The Stanley and Lasalle cultivar extracts also had strong anti-migratory effects. Altogether these onion extracts may contain one or more compounds that may be effective anti-cancer therapies, while the Stanley extract showed the most comprehensive biological activities against Caco-2 cells. https://greenmedinfo.com/article/cytotoxic-effects-stanley-and-fortress-onion-varieties-were-strongest-among-se#comments Colorectal Cancer Onion Anti-metastatic Antiproliferative Anti-metastatic Antiproliferative COLORECTAL CANCER Cultivars Onion In Vitro Study Mon, 10 Jul 2017 22:02:31 +0000 greenmedinfo 150256 at https://greenmedinfo.com