MiR-34a inhibits proliferation and migration of breast cancer through down-regulation of Bcl-2 and SIRT1

Li, Laisheng; Yuan, Linjin; Luo, Jinmei; Gao, Jie; Guo, Jiaoli; Xie, Xiaoming

doi:10.1007/s10238-012-0186-5

Cited by 271 publications

(240 citation statements)

References 38 publications

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“…The results were similar to observations in colon, breast and lung cancer, in which miR-34a expression was downregulated, and overexpression of miR-34a inhibited cell proliferation (7,26,27). The present study selected SIRT1, an energy sensor, to validate the antitumor mechanism of miR-34a in prostate cancer cells.…”

Section: Discussionsupporting

confidence: 88%

miR-34a inhibits cell proliferation in prostate cancer by downregulation of SIRT1 expression

Duan

Zhang

et al. 2015

Oncology Letters

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Abstract. MicroRNA-34a (miR-34a) functions as a tumor suppressor gene and inhibits abnormal cell growth by regulating the expression of other genes. The role of miR-34a in regulating sirtuin 1 (SIRT1) in prostate cancer remains unclear. The objective of the present study was to investigate the biological function and molecular mechanisms of miR-34a regulation of SIRT1 in human prostate cancer samples and the human prostate cancer cell line, PC-3. Fresh prostate tissues were obtained from patients, and the miR-34a expression in prostate cancer tissues was measured using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). qPCR and western blotting were performed to assess the effects of miR-34a overexpression on SIRT1 regulation in PC-3 cells, and the cell growth was assessed by Cell Counting Kit-8 (CCK-8). Flow cytometry was used to assess the cell cycle status of the cells. The miR-34a expression levels in prostate cancer tissues were significantly reduced compared with adjacent normal prostate tissues (P<0.05). SIRT1 expression levels in PC-3 cells with over-expression of miR-34a were significantly reduced compared with those in the negative control (P<0.05). The over-expression of miR-34a inhibited PC-3 cells growth and resulted in increased cell cycle arrest compared with the negative control (P<0.05). In conclusion, miR-34a inhibits the human prostate cancer cell proliferation, in part, through the downregulation of SIRT1 expression.

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Section: Discussionsupporting

confidence: 88%

miR-34a inhibits cell proliferation in prostate cancer by downregulation of SIRT1 expression

Duan

Zhang

et al. 2015

Oncology Letters

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“…49 Therefore, miR34a probably regulates autophagy through Bcl-2/Beclin-1-PI3KIII pathway, via targeting Bcl-2. 21,[50][51][52][53] As indicated in our study, Bcl-2 was upregulated both in mRNA and protein levels in line Figure 8 Overexpression of mir34a by lentivirus vector transfection. Notes: Beas-2B cells were transfected by lentivirus vectors with hsa-mir34a or empty lentiviral vectors for 72 hours.…”

supporting

confidence: 81%

Downregulation of B-cell lymphoma/leukemia-2 by overexpressed microRNA 34a enhanced titanium dioxide nanoparticle-induced autophagy in BEAS-2B cells

Bai¹,

Chen²,

Sun³

et al. 2016

IJN

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Titanium dioxide (TiO 2 ) nanoparticles (TNPs) are manufactured worldwide for a wide range of applications and the toxic effect of TNPs on biological systems is gaining attention. Autophagy is recognized as an emerging toxicity mechanism triggered by nanomaterials. MicroRNA 34a (miR34a) acts as a tumor suppressor gene by targeting many oncogenes, but how it affects autophagy induced by TNPs is not completely understood. Here, we observed the activation of TNP-induced autophagy through monodansylcadaverine staining and LC3-I/LC3-II conversion. Meanwhile, the transmission electron microscope ultrastructural analysis showed typical morphological characteristics in autophagy process. We detected the expression of miR34a and B-cell lymphoma/leukemia-2 (Bcl-2). In addition, the underlying mechanism of TNP-induced autophagy was performed using overexpression of miR34a by lentivirus vector transfection. Results showed that TNPs induced autophagy generation evidently. Typical morphological changes in the process of autophagy were observed by the transmission electron microscope ultrastructural analysis and LC3-I/LC3-II conversion increased significantly in TNP-treated cells. Meanwhile, TNPs induced the downregulation of miR34a and increased the expression of Bcl-2. Furthermore, overexpressed miR34a decreased the expression of Bcl-2 both in messenger RNA and protein level, following which the level of autophagy and cell death rate increased after the transfected cells were incubated with TNPs for 24 hours. These findings provide the first evidence that overexpressed miR34a enhanced TNP-induced autophagy and cell death through targeted downregulation of Bcl-2 in BEAS-2B cells.

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“…Interestingly, miR-34a, a pivotal member of the p53 network, was found to be downregulated in several types of tumor, and was reported to act as a tumor suppressor [31]. In addition, miR-34a inhibited tumor invasion and e Prediction schema of the binding sites between miR-34a and the 3 0 untranslated region of c-Myc.…”

Section: Discussionmentioning

confidence: 99%

Gastrokine 1 inhibits gastric cancer cell migration and invasion by downregulating RhoA expression

et al. 2016

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Background We investigated whether GKN1, a gastric tumor suppressor, contributes to the progression of gastric cancer by regulating RhoA expression. Methods We analyzed the expression of GKN1, RhoA, miR-185, and miR-34a in 35 gastric cancer tissues, and compared their expression with T category and TNM stage. Cell migration and invasion, as well as the expression of epithelial-to-mesenchymal transition (EMT)-related proteins, were assessed in GKN1-and RhoA small interfering RNA (siRhoA)-transfected and recombinant-GKN1-treated AGS and MKN1 gastric cancer cells. Results Expression of RhoA protein and messenger RNA (mRNA) was increased in 15 (42.9 %) and 17 (48.6 %) of 35 gastric cancer tissues respectively, and was associated with higher T category and TNM stage. GKN1 expression was significantly decreased in 27 gastric cancers (77.1 %) with a higher T category, and was inversely correlated with RhoA mRNA expression. In AGS and MKN1 cells, GKN1 expression increased miR-185 and miR-34a expression and reduced RhoA mRNA and protein expression. A positive relationship between GKN1 and miR-34a and miR-185 expression and an inverse relationship between miR-34a and RhoA expression were observed in gastric cancer tissues. Cell migration and invasiveness were markedly decreased in GKN1-and siRhoA-transfected cells. GKN1 expression and silencing of RhoA decreased the expression of the proteins Snail, Slug, and vimentin. Furthermore, miR-185 and miR-34a silencing in MKN1 cells transfected with GKN1 stimulated cell migration and invasion, and increased the expression of EMT-related proteins. Conclusion Our data suggest that GKN1 may inhibit gastric cancer cell migration and invasion by downregulating RhoA expression in a miR-185-and miR-34a-dependent manner.

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MiR-34a inhibits proliferation and migration of breast cancer through down-regulation of Bcl-2 and SIRT1

Cited by 271 publications

References 38 publications

miR-34a inhibits cell proliferation in prostate cancer by downregulation of SIRT1 expression

miR-34a inhibits cell proliferation in prostate cancer by downregulation of SIRT1 expression

Downregulation of B-cell lymphoma/leukemia-2 by overexpressed microRNA 34a enhanced titanium dioxide nanoparticle-induced autophagy in BEAS-2B cells

Gastrokine 1 inhibits gastric cancer cell migration and invasion by downregulating RhoA expression

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