Cisplatin Combined with Metformin Inhibits Migration and Invasion of Human Nasopharyngeal Carcinoma Cells by Regulating E-cadherin and MMP-9

Sun, Xiaojin; Zhang, Pei; Li, Hai-Hui; Jiang, Zhiwen; Jiang, Chenchen; Líu, Hao

doi:10.7314/apjcp.2014.15.9.4019

Cited by 28 publications

(22 citation statements)

References 19 publications

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“…During cancer progression, cancer cells detach from the basement membrane, migrate to and invade surrounding tissues and eventually colonize remote sites (21). A hallmark of cells that have undergone EMT is the loss of the epithelial cell marker E-cadherin and the gain of the mesenchymal cell markers N-cadherin and vimentin (22). Given that the present results revealed that miR-20a increased the EMT-related cell invasion and migration, the next step was to examine the changes in the markers of EMT.…”

Section: Discussionmentioning

confidence: 79%

microRNA-20a enhances the epithelial-to-mesenchymal transition of colorectal cancer cells by modulating matrix metalloproteinases

Jing

Shi

et al. 2015

Experimental and Therapeutic Medicine

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Abstract. The mortality rates associated with colorectal cancer (CRC) are high due to metastasis. Epithelial-to-mesenchymal transition (EMT) is a key step in tumor metastasis. The aim of the present study was to investigate the function of microRNA-20a (miR-20a) in EMT. The expression of miR-20a was analyzed in CRC tissues and cell lines using the reverse transcription-quantitative polymerase chain reaction. Plasmids containing miR-20a short hairpin RNA and miR-20a mimics were transfected into SW620 and LS174T cell lines, respectively. Cell counting kit-8, Transwell ® and wound healing assays were performed to assess the effects of miR-20a on cell proliferation, invasion and migration. EMT markers and matrix metalloproteinases (MMPs) were identified using western blotting. The results showed that increased expression of miR-20a in CRC tissues was associated with tumor invasion and lymph node metastasis (P<0.05). Further experiments indicated that miR-20a-knockdown inhibited the proliferation, invasion and migration of CRC cells, upregulated the expression of vimentin and tissue inhibitor of metalloproteinases-2 (TIMP-2) and downregulated the expression of E-cadherin, MMP-2 and MMP-9. The opposite effects were observed in CRC cell lines overexpressing miR-20a. In conclusion, these results have shown that the upregulation of miR-20a suppresses TIMP-2 expression, which subsequently increases the expression of MMP-2 and MMP-9, thereby promoting the EMT of CRC cells. These findings suggest that miR-20a represents a potential therapeutic target for patients with CRC.

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Section: Discussionmentioning

confidence: 79%

microRNA-20a enhances the epithelial-to-mesenchymal transition of colorectal cancer cells by modulating matrix metalloproteinases

Jing

Shi

et al. 2015

Experimental and Therapeutic Medicine

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“…It had been reported that metformin blocked migration and invasion in some malignancies in vitro [35][36][37][38]. However, whether metformin affects these metastasis-related abilities in osteosarcoma is unclear.…”

Section: Discussionmentioning

confidence: 99%

Metformin inhibits the proliferation, metastasis, and cancer stem-like sphere formation in osteosarcoma MG63 cells in vitro

Zhang

et al. 2015

Tumor Biol.

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Metformin is an oral drug that has been widely used to treat type 2 diabetes mellitus. Interestingly, accumulated evidence indicate that metformin may reduce the risk of cancer in patients with type 2 diabetes and inhibit tumor cell growth and survival in numerous malignancies, including osteosarcoma (OS) cells. In the present study, we aimed to investigate the effects of metformin on the proliferation, migration, invasion, and sphere formation in OS MG63 cells in vitro. Metformin suppressed OS MG63 cell proliferation in a dose- and time-dependent manner and markedly blocked anti-metastatic potentials, migration, and invasion, by downregulating matrix metalloproteinase 2 (MMP2) and MMP9. Besides, we established OS cancer stem-like cell (CSC) model with sarcosphere formation assay and demonstrated that metformin posed damage on CSCs in OS by inhibiting sphere formation and by inducing their stemness loss. The stemness of CSCs in OS such as self-renewal and differentiation potentials was both impaired with a significant decrease of Oct-4 and Nanog activation. Consistent with this, the positive rates of CD90, CD133, and stage-specific embryonic antigen-4 (SSEA-4) were all observed with reductions in response to metformin exposure. In addition, Western blot showed that metformin activated AMPKα at Tyr172, followed by a downregulated phosphorylation of mammalian target of rapamycin (mTOR)/S6 and feedback activation of p-AKT Ser(473) in both OS MG63 cells and CSCs. This indicates that AMPK/mTOR/S6 signaling pathway might be involved in the growth inhibition of both OS MG63 cells and CSCs. These results suggest that metformin, a potential anti-neoplastic agent, might make it a novel therapeutic choice for the treatment of OS in the future.

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“…In a study which aimed to investigate the effects of cisplatin combined with metformin on the proliferation, invasion and migration of HNE1/DDP human nasopharyngeal carcinoma (NPC) cells, and to provide a new target for treating metastasis, it was shown that cisplatin combined with metformin has effects on proliferation, invasion, and migration of human NPC cells (Sun et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

Effects of Metformin on Cell Kinetic Parameters of MCF-7 Breast Cancer Cells in Vitro

Topçul

Çeti̇n²

2015

Asian Pacific Journal of Cancer Prevention

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In this study, the antiproliferative effects of the metformin was evaluated on MCF-7 Cells (human breast adenocarcinoma cell line). For this purpose cell kinetic parameters including cell proliferation assay, mitotic index and labelling index analysis were used. 30 µM, 65 µM and 130 µM Metformin doses were applied to cells for 24, 48 and 72 hours. The results showed that there was a significant decrease in cell proliferation, mitotic index and labelling index for all experimental groups (p<0.05) for all applications.

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Cisplatin Combined with Metformin Inhibits Migration and Invasion of Human Nasopharyngeal Carcinoma Cells by Regulating E-cadherin and MMP-9

Cited by 28 publications

References 19 publications

microRNA-20a enhances the epithelial-to-mesenchymal transition of colorectal cancer cells by modulating matrix metalloproteinases

microRNA-20a enhances the epithelial-to-mesenchymal transition of colorectal cancer cells by modulating matrix metalloproteinases

Metformin inhibits the proliferation, metastasis, and cancer stem-like sphere formation in osteosarcoma MG63 cells in vitro

Effects of Metformin on Cell Kinetic Parameters of MCF-7 Breast Cancer Cells in Vitro

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