Breast Cancer: Bone Metastasis https://greenmedinfo.com/taxonomy/term/5736/all en 1,25(OH)2D inhibits breast cancer cell metastatic capability as well as inhibits EMT, an essential step in the metastatic process. https://greenmedinfo.com/article/125oh2d-inhibits-breast-cancer-cell-metastatic-capability-well-inhibits-emt-es PMID:  Nutr Cancer. 2016 Aug 23:1-8. Epub 2016 Aug 23. PMID: 27552186 Abstract Title:  1α,25-Dihydroxyvitamin D Inhibits the Metastatic Capability of MCF10CA1a and MDA-MB-231 Cells in an In Vitro Model of Breast to Bone Metastasis. Abstract:  Breast cancer metastasis to the bone continues to be a major health problem, with approximately 80% of advanced breast cancer patients expected to develop bone metastasis. Although the problem of bone metastasis persists, current treatment options for metastatic cancer patients are limited. In this study, we investigated the preventive role of the active vitamin D metabolite, 1α,25-dihydroxyvitamin D (1,25(OH)2D), against the metastatic potential of breast cancer cells using a novel three-dimensional model (rMET) recapitulating multiple steps of the bone metastatic process. Treatment of MCF10CA1a and MDA-MB-231 cells inhibited metastasis in the rMET model by 70% (±5.7%)and 21% (±6%), respectively. In addition, 1,25(OH)2D treatment decreased invasiveness (20 ± 11% of vehicle) and decreased the capability of MCF10CA1a cells to survive in the reconstructed bone environment after successful invasion through the basement membrane (69 ± 5% of vehicle). An essentialstep in metastasis is epithelial-mesenchymal transition (EMT). Treatment of MCF10CA1a cells with 1,25(OH)2D increased gene (2.04 ± 0.28-fold increase) and protein (1.87 ± 0.20-fold increase) expression of E-cadherin. Additionally, 1,25(OH)2D treatment decreased N-cadherin gene expression (42 ± 8%decrease), a marker for EMT. Collectively, the present study suggests that 1,25(OH)2D inhibits breast cancer cell metastatic capability as well as inhibits EMT, an essential step in the metastatic process. https://greenmedinfo.com/article/125oh2d-inhibits-breast-cancer-cell-metastatic-capability-well-inhibits-emt-es#comments Breast Cancer Breast Cancer: Bone Metastasis Breast Cancer: Triple Negative Vitamin D Anti-metastatic In Vitro Study Wed, 24 Aug 2016 14:33:29 +0000 greenmedinfo 133873 at https://greenmedinfo.com Blueberry anthrocyanins exhibit anticancer and anti-invasive properties in breast cancer cell lines. https://greenmedinfo.com/article/blueberry-anthrocyanins-exhibit-anticancer-and-anti-invasive-properties-breast PMID:  Phytother Res. 2010 Jun 17. Epub 2010 Jun 17. PMID: 20564502 Abstract Title:  Blueberry anthocyanins and pyruvic acid adducts: anticancer properties in breast cancer cell lines. Abstract:  The purpose of this study was to investigate the anticancer properties of an anthocyanin-pyruvic acid adduct extract, which is being developed aiming to be further applied in the food industry. An anthocyanin extract from blueberry (extract I) and an anthocyanin-pyruvic acid adduct extract (extract II) were tested on two breast cancer cell lines (MDA-MB-231 and MCF7). Proliferation was assessed by SRB assay and (3)H-thymidine incorporation. Caspase-3 activity was determined in the presence of both extracts. Their capacity as chemoattractants and their invasive potential were also assayed.In both cell lines, extracts I and II significantly reduced cell proliferation at 250 mug/mL, after 24 h of cell incubation. Caspase-3 activity was not altered by the extracts (250 mug/mL) in either cell line, with the exception of extract II in MCF-7, which increased its activity, probably explaining its effects on cell proliferation.Both extracts (250 mug/mL) demonstrated significant antiinvasive potential in both cell lines. Furthermore, they did not demonstrate any capacity for chemotaxis.In conclusion, blueberry anthocyanins and the respective anthocyanin-pyruvic acid adducts demonstrated anticancer properties by inhibiting cancer cell proliferation and by acting as cell antiinvasive factors and chemoinhibitors. The anthocyanin-pyruvic acid adduct extract showed a more pronounced effect in MDA-MB-231, suggesting an effect independent of estrogen receptors. Copyright (c) 2010 John Wiley&amp;Sons, Ltd. https://greenmedinfo.com/article/blueberry-anthrocyanins-exhibit-anticancer-and-anti-invasive-properties-breast#comments Blueberry Breast Cancer Breast Cancer: Bone Metastasis Breast Cancer: Invasive Lobular Carcinoma (ILC) Breast Cancer: Lung Metastasis Breast Cancer: Metastatic Cancer Metastasis Anti-metastatic In Vitro Study Thu, 16 Sep 2010 12:17:36 +0000 greenmedinfo 56626 at https://greenmedinfo.com Bone-protective and anti-tumor effect of baicalin in osteotropic breast cancer via induction of apoptosis. https://greenmedinfo.com/article/bone-protective-and-anti-tumor-effect-baicalin-osteotropic-breast-cancer-induc PMID:  Breast Cancer Res Treat. 2020 Dec ;184(3):711-721. Epub 2020 Sep 16. PMID: 32939591 Abstract Title:  Bone-protective and anti-tumor effect of baicalin in osteotropic breast cancer via induction of apoptosis. Abstract:  PURPOSE: Research suggested that bone is the specific target organ for breast cancer metastasis. The related tumor causes significant morbidity due to a reduction in quality of life and physical function. Increased osteoclast function is implicated in the bone microenvironment during the outgrowth of breast cancer. In the present experimental study, we examined the potential bone-protective effect of baicalin osteotropic breast Cancer and explored the possible mechanism of action.METHODS: In vitro cell viability effect of baicalin was assessed on the breast cancer cell lines (MDA-MB-231 and MCF-7). We also estimated the in vitro osteoclast and bone resorption. Further, baicalin-regulated osteoblastogenesis and osteoclastogenesis were also estimated in vitro. Finally, the role of the baicalin in the expansion of osteolytic bone disease was scrutinized in a breast cancer bone metastases model.RESULTS: Baicalin significantly (p <p><a href="https://greenmedinfo.com/article/bone-protective-and-anti-tumor-effect-baicalin-osteotropic-breast-cancer-induc" target="_blank">read more</a></p> https://greenmedinfo.com/article/bone-protective-and-anti-tumor-effect-baicalin-osteotropic-breast-cancer-induc#comments Breast Cancer Breast Cancer: Bone Metastasis Flavonoids Apoptotic Osteoprotective In Vitro Study Thu, 04 Nov 2021 22:18:11 +0000 greenmedinfo 248264 at https://greenmedinfo.com Curcumin inhibits inflammation-induced bone resportion that is frequently associated with cancers such as metastatic breast cancer and multiple myeloma. https://greenmedinfo.com/article/curcumin-inhibits-inflammation-induced-bone-resportion-frequently-associated-c PMID:  Ann Rheum Dis. 1995 Jun;54(6):491-3. PMID: 15128775 Abstract Title:  Curcumin (diferuloylmethane) inhibits receptor activator of NF-kappa B ligand-induced NF-kappa B activation in osteoclast precursors and suppresses osteoclastogenesis. Abstract:  Numerous studies have indicated that inflammatory cytokines play a major role in osteoclastogenesis, leading to the bone resorption that is frequently associated with cancers and other diseases. Gene deletion studies have shown that receptor activator of NF-kappaB ligand (RANKL) is one of the critical mediators of osteoclastogenesis. How RANKL mediates osteoclastogenesis is not fully understood, but an agent that suppresses RANKL signaling has potential to inhibit osteoclastogenesis. In this report, we examine the ability of curcumin (diferuloylmethane), a pigment derived from turmeric, to suppress RANKL signaling and osteoclastogenesis in RAW 264.7 cells, a murine monocytic cell line. Treatment of these cells with RANKL activated NF-kappaB, and preexposure of the cells to curcumin completely suppressed RANKL-induced NF-kappaB activation. Curcumin inhibited the pathway leading from activation of IkappaBalpha kinase and IkappaBalpha phosphorylation to IkappaBalpha degradation. RANKL induced osteoclastogenesis in these monocytic cells, and curcumin inhibited both RANKL- and TNF-induced osteoclastogenesis and pit formation. Curcumin suppressed osteoclastogenesis maximally when added together with RANKL and minimally when it was added 2 days after RANKL. Whether curcumin inhibits RANKL-induced osteoclastogenesis through suppression of NF-kappaB was also confirmed independently, as RANKL failed to activate NF-kappaB in cells stably transfected with a dominant-negative form of IkappaBalpha and concurrently failed to induce osteoclastogenesis. Thus overall these results indicate that RANKL induces osteoclastogenesis through the activation of NF-kappaB, and treatment with curcumin inhibits both the NF-kappaB activation and osteoclastogenesis induced by RANKL. https://greenmedinfo.com/article/curcumin-inhibits-inflammation-induced-bone-resportion-frequently-associated-c#comments Breast Cancer: Bone Metastasis Curcumin Multiple Myeloma Enzyme Inhibitors NF-kappaB Inhibitor In Vitro Study Sat, 16 Jan 2010 17:13:11 +0000 greenmedinfo 49451 at https://greenmedinfo.com Curcumin inhibits metastatic breast cancer cells. https://greenmedinfo.com/article/curcumin-inhibits-metastatic-breast-cancer-cells PMID:  Front Oncol. 2012 ;2:161. Epub 2012 Nov 15. PMID: 23162792 Abstract Title:  Modulating the vascular behavior of metastatic breast cancer cells by curcumin treatment. Abstract:  The spreading of tumor cells to secondary sites (tumor metastasis) is a complex process that involves multiple, sequential steps. Vascular adhesion and extravasation of circulating tumor cells (CTCs) is one, critical step. Curcumin, a natural compound extracted from Curcuma longa, is known to have anti-tumoral, anti-proliferative, anti-inflammatory properties and affect the expression of cell adhesion molecules, mostly by targeting the NF-κB transcription factor. Here, upon treatment with curcumin, the vascular behavior of three different estrogen receptor negative (ER(-)) breast adenocarcinoma cell lines (SK-BR-3, MDA-MB-231, MDA-MB-468) is analyzed using a microfluidic system. First, the dose response to curcumin is characterizedat 24, 48, and 72 h using a XTT assay. For all three cell lines, an IC(50) larger than 20 µM is observed at 72 h; whereas no significant reduction in cell viability is detected for curcumin concentrations up to 10 µM. Upon 24 h treatment at 10 µM of curcumin, SK-BR3 and MDA-MB-231 cells show a decrease in adhesion propensity of 40% (p = 0.02) and 47% (p = 0.001), respectively. No significant change is documented for the less metastatic MDA-MB-468 cells. All three treated cell lines show a 20% increase in rolling velocity from 48.3 to 58.7 µm/s in SK-BR-3, from 64.1 to 73.77 µm/s in MDA-MB-231, and from 57.5 to 74.4 µm/s in MDA-MB-468. Collectively, these results suggest that mild curcumin treatments could limit the metastatic potential of these adenocarcinoma cell lines, possibly by altering the expression of adhesion molecules, and the organization and stiffness of the cell cytoskeleton. Future studies will elucidate the biophysical mechanisms regulating this curcumin-induced behavior and further explore the clinical relevance of these findings. https://greenmedinfo.com/article/curcumin-inhibits-metastatic-breast-cancer-cells#comments Breast Cancer: Bone Metastasis Breast Cancer: Metastatic Cancer Metastasis Curcumin In Vitro Study Wed, 12 Dec 2012 22:37:06 +0000 greenmedinfo 86609 at https://greenmedinfo.com Effect of aluminium on migratory and invasive properties of MCF-7 human breast cancer cells in culture. https://greenmedinfo.com/article/effect-aluminium-migratory-and-invasive-properties-mcf-7-human-breast-cancer-c PMID:  J Inorg Biochem. 2013 Jul 12. Epub 2013 Jul 12. PMID: 23896199 Abstract Title:  Effect of aluminium on migratory and invasive properties of MCF-7 human breast cancer cells in culture. Abstract:  Aluminium (Al) has been measured in human breast tissue, nipple aspirate fluid and breast cyst fluid, and recent studies have shown that at tissue concentrations, aluminium can induce DNA damage and suspension growth in human breast epithelial cells. This paper demonstrates for the first time that exposure to aluminium can also increase migratory and invasive properties of MCF-7 human breast cancer cells. Long-term (32weeks) but not short-term (1week) exposure of MCF-7 cells to 10(-4)M aluminium chloride or 10(-4)M aluminium chlorohydrate increased motility of the cells as measured by live cell imaging (cumulative length moved by individual cells), by a wound healing assay and by migration in real time through 8μm pores of a membrane using xCELLigence technology. Long-term exposure (37weeks) to 10(-4)M aluminium chloride or 10(-4)M aluminium chlorohydrate also increased the ability of MCF-7 cells to invade through a matrigel layer as measured in real time using the xCELLigence system. Although molecular mechanisms remain to be characterized, the ability of aluminium salts to increase migratory and invasive properties of MCF-7 cells suggests that the presence of aluminium in the human breast could influence metastatic processes. This is important because mortality from breast cancer arises mainly from tumour spread rather than from the presence of a primary tumour in the breast. https://greenmedinfo.com/article/effect-aluminium-migratory-and-invasive-properties-mcf-7-human-breast-cancer-c#comments Breast Cancer Breast Cancer: Bone Metastasis Carcinogenic In Vitro Study Wed, 04 Sep 2013 16:49:33 +0000 greenmedinfo 109649 at https://greenmedinfo.com Flaxseed Helps Prevent And Kill Breast Cancer, Meta-Analysis Reveals https://greenmedinfo.com/blog/flaxseed-can-prevent-and-kill-breast-cancer-meta-analysis-confirms-1 <div class="copyright">This article is copyrighted by GreenMedInfo LLC, 2020<br/><strong><a href="/greenmedinfocom-re-post-guidelines">Visit our Re-post guidelines</a></strong></div><p class="rtecenter"><img alt="Flaxseed Can Prevent And Kill Breast Cancer, Meta-Analysis Reveals" src="//cdn.greenmedinfo.com/sites/default/files/ckeditor/Sayer Ji/images/flaxseed_kills_breast_cancer.jpg" style="height: 385px; width: 575px;" /></p> <p>As we edge closer toward Breast Cancer Awareness month,<a href="#_ftn1" name="_ftnref1" title="">[1]</a> one cause that most likely won't be marketed to us is that of women taking back control of their health by consuming more cancer-fighting foods.&nbsp;</p> <p>In years past, Smith &amp; Wesson's pink hand gun and KFC's "buckets for the cure,"<a href="#_ftn2" name="_ftnref2" title="">[2]</a> have made the list of approved 'pink' products, but nowhere does one find fund-raisers and races for better access to and consumption of the extensive list of foods that increasingly science has vetted as actually preventing and/or killing breast cancer. <a href="#_ftn3" name="_ftnref3" title="">[3]</a>&nbsp; &nbsp;</p><p><a href="https://greenmedinfo.com/blog/flaxseed-can-prevent-and-kill-breast-cancer-meta-analysis-confirms-1" target="_blank">read more</a></p> https://greenmedinfo.com/blog/flaxseed-can-prevent-and-kill-breast-cancer-meta-analysis-confirms-1#comments Breast Cancer Breast Cancer: Bone Metastasis Breast Cancer: Chemically-Induced Breast Cancer: Diagnosis Breast Cancer: Drug Resistant Breast Cancer: Ductal Carcinoma In Situ Breast Cancer: Estrogen Flaxseed Chemopreventive Chemotherapeutic Health Guide: Breast Cancer Wed, 11 Sep 2013 12:51:48 +0000 Sayer Ji 109696 at https://greenmedinfo.com Fructose consumption may worsen the condition of breast cancer patients. https://greenmedinfo.com/article/fructose-consumption-may-worsen-condition-breast-cancer-patients PMID:  Int J Oncol. 2010 Sep;37(3):615-22. PMID: 20664930 Abstract Title:  Fructose as a carbon source induces an aggressive phenotype in MDA-MB-468 breast tumor cells. Abstract:  Aberrant glycosylation is a universal feature of cancer cells, and certain glycan structures are well-known markers for tumor progression. Availability and composition of sugars in the microenvironment may affect cell glycosylation. Recent studies of human breast tumor cell lines indicate their ability to take up and utilize fructose. Here we tested the hypothesis that adding fructose to culture as a carbon source induces phenotypic changes in cultured human breast tumor cells that are associated with metastatic disease. MDA-MB-468 cells were adapted to culture media in which fructose was substituted for glucose. Changes in cell surface glycan structures, expression of genes related to glycan assembly, cytoskeleton F-actin, migration, adhesion and invasion were determined. Cells cultured in fructose expressed distinct cell-surface glycans. The addition of fructose affected sialylation and fucosylation patterns. Fructose feeding also increased binding of leukoagglutinating Phaseolus vulgaris isolectin, suggesting a possible rise in expression of branching beta-1, 6 GlcNAc structures. Rhodamine-phalloidin staining revealed an altered F-actin cytoskeletal system. Fructose accelerated cellular migration and increased invasion. These data suggest that changing the carbon source of the less aggressive MDA-MB-468 cell line induced characteristics associated with more aggressive phenotypes. These data could be of fundamental importance due to the markedly increased consumption of sweeteners containing free fructose in recent years, as they suggest that the presence of fructose in nutritional microenvironment of tumor cells may negatively affect the outcome for some breast cancer patients. https://greenmedinfo.com/article/fructose-consumption-may-worsen-condition-breast-cancer-patients#comments Breast Cancer Breast Cancer: Bone Metastasis Breast Cancer: Invasive Lobular Carcinoma (ILC) Breast Cancer: Metastatic Breast Cancer: Prevention Breast Cancer: Recovery Breast Cancer: Triple Negative Fructose High Fructose Corn Syrup Human Study Tue, 03 Aug 2010 20:07:28 +0000 greenmedinfo 55880 at https://greenmedinfo.com Guggul may inhibit the progression of cancers such as multiple myeloma and breast cancer by modulating inflammation and tumor cell-induced osteoclastogenesis. https://greenmedinfo.com/article/guggul-may-inhibit-progression-cancers-such-multiple-myeloma-and-breast-cancer PMID:  J Nerv Ment Dis. 2007 Jun;195(6):504-13. PMID: 16428513 Abstract Title:  Guggulsterone inhibits osteoclastogenesis induced by receptor activator of nuclear factor-kappaB ligand and by tumor cells by suppressing nuclear factor-kappaB activation. Abstract:  Bone resorption is commonly associated with aging and with certain types of cancer, including multiple myeloma and breast cancer. What induces bone resorption is not fully understood, but the role of osteoclasts is well established. Recently, receptor activator of nuclear factor-kappaB (NF-kappaB) ligand (RANKL), a member of the tumor necrosis factor superfamily, was implicated as a major mediator of bone resorption, suggesting that agents that can suppress RANKL signaling have the potential to inhibit bone resorption or osteoclastogenesis. Guggulsterone [4,17(20)-pregnadiene-3,16-dione], isolated from the guggul tree Commiphora mukul and used to treat osteoarthritis and bone fractures, was recently shown to antagonize the farnesoid X receptor, decrease the expression of bile acid-activated genes, and suppress the NF-kappaB activation induced by various carcinogens. We investigated whether guggulsterone could modulate RANKL signaling and osteoclastogenesis induced by RANKL or tumor cells. We found that treatment of monocytes with guggulsterone suppressed RANKL-activated NF-kappaB activation (as indicated by gel-shift assay) and that this suppression correlated with inhibition of IkappaBalpha kinase and phosphorylation and degradation of IkappaBalpha, an inhibitor of NF-kappaB. Guggulsterone also suppressed the differentiation of monocytes to osteoclasts in a dose-dependent and time-dependent manner. Suppression of osteoclastogenesis by the NF-kappaB-specific inhibitory peptide implies a link between NF-kappaB and osteoclastogenesis. Finally, differentiation to osteoclasts induced by coincubating human breast tumor cells (MDA-MB-468) or human multiple myeloma (U266) cells with monocytes was also completely suppressed by guggulsterone. Collectively, our results indicate that guggulsterone suppresses RANKL and tumor cell-induced osteoclastogenesis by suppressing the activation of NF-kappaB. https://greenmedinfo.com/article/guggul-may-inhibit-progression-cancers-such-multiple-myeloma-and-breast-cancer#comments Breast Cancer: Bone Metastasis Guggul Multiple Myeloma Anti-Tumor NF-kappaB Inhibitor In Vitro Study Sat, 16 Jan 2010 17:07:34 +0000 greenmedinfo 49450 at https://greenmedinfo.com Indole-3 carbinol, a compound found in cabbage, may prevent and treat breast cancer bone metastasis. https://greenmedinfo.com/article/indole-3-carbinol-compound-found-cabbage-may-prevent-and-treat-breast-cancer-b PMID:  Mol Cancer Ther. 2006 Nov;5(11):2747-56. PMID: 17121921 Abstract Title:  Therapeutic intervention of experimental breast cancer bone metastasis by indole-3-carbinol in SCID-human mouse model. Abstract:  Several lines of experimental evidence have suggested that chemokine receptor CXCR4, a metastasis-promoting molecule, may play important roles in breast cancer bone metastasis. There is emerging evidence linking CXCR4 to matrix metalloproteinases (MMP) as well as their regulator nuclear factor-kappaB (NF-kappaB), a key transcription factor, which is known to activate metastasis-promoting molecules for many types of malignancies, including breast cancer. A recent study also showed that promoter region of CXCR4 has several NF-kappaB-binding sites, suggesting that there may be a cross-talk between CXCR4 and NF-kappaB. We have shown previously that indole-3-carbinol (I3C), a natural compound present in vegetables of the genus Brassica, can inhibit NF-kappaB in breast cancer cells. However, there are no reports in the literature showing any effect of I3C on CXCR4 expression in vitro and in vivo. We therefore examined whether I3C could inhibit bone metastasis of breast cancer by inhibiting CXCR4 and MMP-9 expression mediated via the inhibition of the NF-kappaB signaling pathway. Here, we have modified the severe combined immunodeficient (SCID)-human mouse model of experimental bone metastasis for use with the MDA-MB-231 breast cancer cell line. In this animal model, we found that I3C significantly inhibited MDA-MB-231 bone tumor growth, and our results were correlated with the down-regulation of NF-kappaB. Moreover, we found that I3C significantly inhibited the expression of multiple genes involved in the control of metastasis and invasion in vitro and in vivo, especially the expression of CXCR4 and MMP-9 along with pro-MMP-9, with concomitant decrease in Bcl-2 and increase in the proapoptotic protein Bax. From these results, we conclude that the CXCR4/NF-kappaB pathway is critical during I3C-induced inhibition of experimental breast cancer bone metastasis. These results also suggest that I3C could be a promising agent for the prevention and/or treatment of breast cancer bone metastasis in the future. https://greenmedinfo.com/article/indole-3-carbinol-compound-found-cabbage-may-prevent-and-treat-breast-cancer-b#comments Breast Cancer: Bone Metastasis Cabbage Indole-3-Carbinol Animal Study Tue, 19 May 2009 20:38:52 +0000 greenmedinfo 44380 at https://greenmedinfo.com Ipriflavone inhibits the growth of cancer cells and bone metastasis of human breast cancer. https://greenmedinfo.com/article/ipriflavone-inhibits-growth-cancer-cells-and-bone-metastasis-human-breast-canc PMID:  Life Sci. 2004 Aug 27;75(15):1817-31. PMID: 12115517 Abstract Title:  Ipriflavone inhibits osteolytic bone metastasis of human breast cancer cells in a nude mouse model. Abstract:  Osteolytic bone metastasis is a frequent problem in the treatment of cancer. Ipriflavone, a synthetic isoflavone that inhibits osteoclastic bone resorption, has been used for the treatment of osteoporosis in some countries. Some other isoflavones also exhibit an antitumor effect in vitro and in vivo. Here, we studied the effects of ipriflavone on osteolytic bone metastasis of MDA-231 human breast cancer cells injected intracardially into athymic nude mice (ICR-nu/nu). Daily oral administration of ipriflavone at 12 mg/mouse significantly inhibited the development of new osteolytic bone metastases (p &lt; 0.05) and the progression of established osteolytic lesions (p = 0.01), prolonging the life of tumor-bearing mice (p = 0.01 vs. control). In addition, ipriflavone reduced the number of osteoclasts at the bone-cancer interface with no severe adverse effects on the host. In vitro, ipriflavone inhibited the proliferation and DNA synthesis of MDA-231 cells and blocked the ligand-induced phosphorylation of Tyr(845) of the EGFR. Ipriflavone did not promote apoptosis of MDA-231 cells. Our results show that ipriflavone not only directly inhibits the growth of cancer cells but also reduces osteoclasts to prevent the soft tissue tumor burden and osteolytic bone metastases. These findings raise the possibility that ipriflavone may be of use as a therapeutic agent against osteolytic bone metastasis. Copyright 2002 Wiley-Liss, Inc.   https://greenmedinfo.com/article/ipriflavone-inhibits-growth-cancer-cells-and-bone-metastasis-human-breast-canc#comments Breast Cancer Breast Cancer: Bone Metastasis Ipriflavone Animal Study Mon, 20 Apr 2009 06:10:08 +0000 greenmedinfo 41735 at https://greenmedinfo.com Oleuropein Induces Anti-metastatic Effects in Breast Cancer. https://greenmedinfo.com/article/oleuropein-induces-anti-metastatic-effects-breast-cancer PMID:  Asian Pac J Cancer Prev. 2012 ;13(9):4555-9. PMID: 23167379 Abstract Title:  Oleuropein Induces Anti-metastatic Effects in Breast Cancer. Abstract:  Breast cancer causes death due to distant metastases in which tumor cells produce matrix metalloproteinase (MMP) enzymes which facilitate invasion. Oleuropein, the main olive oil polyphenol, has anti-proliferative effects. This study aimed to investigate the effect of oleuropein on the metastatic and anti-metastatic gene expression in the MDA human breast cancer cell line. We evaluated the MMPs and TIMPs gene expression by semi-quantitative reverse transcriptase polymerase chain reaction (RT-PCR) in treated and untreated cells. This study demonstrated that OL may induce anti-metastatic effects on human breast cancer cells. We found that TIMP1,-3, and -4 were over-expressed after all periods of incubation in treated cancer cells compared to untreated cells, while MMP2 and MMP9 genes were down-regulated, at least initially. Treatment of breast cancer cells with oleuropein could help in prevention of cancer metastasis by increasing the TIMPs and suppressing the MMPs gene expressions. https://greenmedinfo.com/article/oleuropein-induces-anti-metastatic-effects-breast-cancer#comments Breast Cancer Breast Cancer: Bone Metastasis Oleuropein Anti-metastatic Matrix metalloproteinase-2 (MMP-2) inhibitor Matrix metalloproteinase-9 (MMP-9) inhibitor In Vitro Study Fri, 30 Nov 2012 22:14:01 +0000 greenmedinfo 85754 at https://greenmedinfo.com Pogostone attenuates osteolysis in breast cancer. https://greenmedinfo.com/article/pogostone-attenuates-osteolysis-breast-cancer PMID:  Life Sci. 2023 Sep 1 ;328:121611. Epub 2023 Apr 15. PMID: 37068706 Abstract Title:  Pogostone attenuates osteolysis in breast cancer by inhibiting the NF-kB and JNK signaling pathways of osteoclast. Abstract:  AIMS: Breast cancer is the most prevalent cancer in females, and approximately 70 % of all patients have evidence of metastatic bone disease, which substantially affects the quality of life and survival rate of breast cancer patients. Osteoporosis has become a global public health problem, and the abnormal activation of osteoclasts is the key to the progression of osteoporosis and the key to both diseases lies in the osteoclasts. Effective drug treatments are lacking and there is an urgent need to explore new drugs.MATERIALS AND METHODS: We observed the effects of pogostone (PO) on osteoclast differentiation, bone resorption function and other indicators, and F-actin ring formation by using Trap staining, SEM and immunofluorescence, and further explored the targets of pogostone in regulating osteoclast differentiation and function using qPCR and Western Blot. In addition, we used CCK 8, Transwell, and flow cytometry to study the effects of pogostone on proliferation, invasion, migration, and apoptosis of MDA-MB-231 cells. Animal models were also constructed for in vivo validation.KEY FINDINGS: Pogostone inhibits osteoclast differentiation, bone resorption, formation of F-actin ring, and the expression of specific genes by attenuated NF-kB degradation and phosphorylation of JNK. In vitro, pogostone suppresses invasion of breast cancer cells, migration, and promotes their apoptosis. In mouse models, pogostone attenuated osteoclast formation and bone resorption, blocked breast cancer cells migration, and supprsed breast cancer-induced osteolysis and ovariectomized (OVX)-mediated osteoporosis.SIGNIFICANCE: These biological functions of pogostone make it a potential drug for treatment of breast cancer-associated bone metastasis in the future. <p><a href="https://greenmedinfo.com/article/pogostone-attenuates-osteolysis-breast-cancer" target="_blank">read more</a></p> https://greenmedinfo.com/article/pogostone-attenuates-osteolysis-breast-cancer#comments Breast Cancer: Bone Metastasis Patchouli Anti-metastatic Apoptotic Animal Study Sat, 09 Sep 2023 17:17:00 +0000 greenmedinfo 280063 at https://greenmedinfo.com Proanthocyanidins attenuate breast cancer-induced bone metastasis by inhibiting Irf-3/c-jun activation. https://greenmedinfo.com/article/proanthocyanidins-attenuate-breast-cancer-induced-bone-metastasis-inhibiting-i PMID:  Anticancer Drugs. 2019 Oct 22. Epub 2019 Oct 22. PMID: 31651438 Abstract Title:  Proanthocyanidins attenuate breast cancer-induced bone metastasis by inhibiting Irf-3/c-jun activation. Abstract:  We have previously demonstrated the pivotal role of Jnk-mediated Irf-3/c-Jun in regulating nuclear factor kappa-Β ligand (RANKL)-induced osteoclastogenesis. Here, we demonstrated that proanthocyanidins (PACs) target Irf-3 to alleviate breast cancer-induced activation of osteoclasts. We also found that PACs induced apoptosis of osteoclast precursors by upregulating the ratio of bax/bcl-2 and activating caspase-3 activity. Such bone protective effect also could be observed in a bone metastasis model of breast cancer. These findings provided a novel therapeutic intervention targeting abnormal bone metabolism to alleviate bone metastasis of breast cancer. <p><a href="https://greenmedinfo.com/article/proanthocyanidins-attenuate-breast-cancer-induced-bone-metastasis-inhibiting-i" target="_blank">read more</a></p> https://greenmedinfo.com/article/proanthocyanidins-attenuate-breast-cancer-induced-bone-metastasis-inhibiting-i#comments Breast Cancer: Bone Metastasis Proanthocyanidins Anti-metastatic In Vitro Study Fri, 24 Jan 2020 00:21:05 +0000 greenmedinfo 209091 at https://greenmedinfo.com Thymoquinone inhibits bone metastasis of breast cancer cells. https://greenmedinfo.com/article/thymoquinone-inhibits-bone-metastasis-breast-cancer-cells PMID:  Front Pharmacol. 2018 ;9:1294. Epub 2018 Dec 4. PMID: 30564115 Abstract Title:  Thymoquinone Inhibits Bone Metastasis of Breast Cancer Cells Through Abrogation of the CXCR4 Signaling Axis. Abstract:  Overexpression of chemokine receptor type 4 (CXCR4) has been found to be associated with increased cell proliferation, metastasis and also act as an indicator of poor prognosis in patients with breast cancer. Therefore, new agents that can abrogate CXCR4 expression have potential against breast cancer metastasis. In this study, we examined the potential effect of thymoquinone (TQ), derived from the seeds of, on the expression and regulation of CXCR4 in breast cancer cells. TQ was found to inhibit the expression of CXCR4 in MDA-MB-231 triple negative breast cancer (TNBC) cells in a dose- and time-dependent manner. It was noted that suppression of CXCR4 by TQ was possibly transcriptionally regulated, as treatment with this drug caused down-regulation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation and suppression of NF-κB binding to the CXCR4 promoter. Pretreatment with a proteasome inhibitor and/or lysosomal stabilization did not affect TQ induced suppression of CXCR4. Down-regulation of CXCR4 was further correlated with the inhibition of CXCL12-mediated migration and invasion of MDA-MB-231 cells. Interestingly, it was observed that the deletion of p65 could reverse the observed anti-invasive/anti-migratory effects of TQ in breast cancer cells. TQ also dose-dependently inhibited MDA-MB-231 tumor growth and tumor vascularity in a chick chorioallantoic membrane assay model. We also observed TQ (2 and 4 mg/kg) treatment significantly suppressed multiple lung, brain, and bone metastases in a dose-dependent manner in a metastasis breast cancer mouse model. Interestingly, H&amp;E and immunohistochemical analysis of bone isolated from TQ treated mice indicated a reduction in number of osteolytic lesions and the expression of metastatic biomarkers. In conclusion, the results indicate that TQ primarily exerts its anti-metastatic effects by down-regulation of NF-κB regulated CXCR4 expression and thus has potential for the treatment of breast cancer. <p><a href="https://greenmedinfo.com/article/thymoquinone-inhibits-bone-metastasis-breast-cancer-cells" target="_blank">read more</a></p> https://greenmedinfo.com/article/thymoquinone-inhibits-bone-metastasis-breast-cancer-cells#comments Breast Cancer: Bone Metastasis Thymoquinone Anti-metastatic NF-kappaB Inhibitor In Vitro Study Fri, 11 Jan 2019 02:26:01 +0000 greenmedinfo 177312 at https://greenmedinfo.com