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Abstract Title:

Curcumin inhibits cell proliferation and induces apoptosis of human non-small cell lung cancer cells through the upregulation of miR-192-5p and suppression of PI3K/Akt signaling pathway.

Abstract Source:

Oncol Rep. 2015 Sep 8. Epub 2015 Sep 8. PMID: 26351877

Abstract Author(s):

Hai Jin, Fan Qiao, Yan Wang, Yongdong Xu, Yan Shang

Article Affiliation:

Hai Jin

Abstract:

Curcumin is the main active ingredient extracted from the traditional Chinese medicine, turmeric, which acts against non-small cell lung cancer cell (NSCLC), lowers blood pressure, is anti-inflammatory, choleretic, and exerts anti‑oxidant effects, without any obvious toxicity in the long term. The aim of the present study was to investigate whether the anticancer effect of curcumin inhibited cell proliferation and induced apoptosis of human NSCLC through the upregulation of microRNA‑192-5p (miR-192-5p) and suppression ofthe PI3K/Akt signaling pathway. In the present study, treatment with curcumin inhibited cell proliferation, induced cell apoptosis and increased the caspase-3 activity of A549 cells. The results also showed that, miR-192-5p relative expression of NCL-H460 cells was relatively lower than that of A549 cells, which was higher, with that of BEAS-2E cells being the highest. miR-192-5p mimics suppressed cell proliferation and increased cell apoptosis of A549 cells. However, anti-miR-192-5p mimics increased cell proliferation and inhibited cell apoptosis of A549 cells. Curcumin treatment effectivelyincreased the relative miR‑192-5p expression and suppressed the PI3K/Akt signaling pathway. miR-192-5p mimics enhanced the effect of curcumin on cell viability and apoptosis and suppressed the PI3K/Akt signaling pathway in A549 cells. Anti-miR-192-5p mimics reversed the effect of curcumin on A549cells and PI3K/Akt expression. Collectively, our findings suggested that curcumin inhibited cell proliferation and induced apoptosis of human non-small cell lung cancer cells through the upregulation of miR-192-5p and suppression of the PI3K/Akt signaling pathway.

Study Type : In Vitro Study

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Sayer Ji
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