RNA interference of metastasis‐associated gene 1 inhibits metastasis of B16F10 melanoma cells in a C57BL/6 mouse model

Qian, Haili; Yu, Jing; Li, Yunfeng; Wang, Haijuan; Song, Chongwen; Zhang, Xueyan; Liang, Xiao; Fu, Ming; Chen, Lin

doi:10.1042/bc20060130

Cited by 33 publications

(19 citation statements)

References 24 publications

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“…These in vitro studies provide evidence that MTA1 may play important roles in lung cancer development. Our results are consistent with the in vitro studies on esophageal carcinoma cells and melanoma cells performed by Qian et al (19,20). MTA1 downregulation greatly reversed the malignant phenotypes of cancer cells.…”

Section: Discussionsupporting

confidence: 82%

MTA1 gene silencing inhibits invasion and alters the microRNA expression profile of human lung cancer cells

et al. 2012

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Abstract. Metastasis-associated gene 1 (MTA1) is involved in the carcinogenesis and metastasis of many human carcinomas. However, its exact role in non-small cell lung cancer (NSCLC) is still unclear. Using immunohistochemistry analysis, we recently identified MTA1 to be associated with the progression of NSCLC. Here, we carried out further analysis on the effect of MTA1 knockdown in an NSCLC cell line on cell functions and the global microRNA (miRNA) expression profile. We succeeded in establishing the MTA1 knockdown NSCLC cell line using RNA interference (RNAi), and found that the silencing of MTA1 resulted in the effective inhibition of the invasive ability of NSCLC cells, but not of the cell growth in vitro. We performed an miRNA microarray analysis and demonstrated for the first time that MTA1 knockdown significantly changed the expression of some miRNAs in NSCLC cells. Among them, some have a well-characterized association with cancer progression, e.g. miR-125b, miR-210, miR-103, miR-194 and miR-500. In summary, it is evident from our results that MTA1 functions in regulating the invasive phenotype of lung cancer cells and this regulation may be through altered miRNA expression. The interaction between MTA1 and the miRNAs which contributes to lung cancer is worthy of further investigation.

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Section: Discussionsupporting

confidence: 82%

MTA1 gene silencing inhibits invasion and alters the microRNA expression profile of human lung cancer cells

et al. 2012

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“…Therefore, it was hypothesized that there is a certain inherent connection between E-cadherin and MTA1, and their coordination may lead to tumor cell invasion and metastasis. E-cadherin may be upregulated by MTA1 siRNA in melanoma cells, which was also confirmed in our previous study in cervical cancer cells (29,30). MTA1 overexpression resulted in the downregulation of E-cadherin expression in ovarian cancer (23).…”

Section: Discussionsupporting

confidence: 64%

“…Moreover, MTA1 has been identified to determine EMT phenotypes mainly through downregulating the expression of E-cadherin, which leads to EMT (27,28). E-cadherin can be upregulated using MTA1 small interfering RNA (siRNA) in melanoma cells, which was also confirmed in our previous study in cervical cancer cells (29,30). MTA1 and E-cadherin are involved in the EMT process (28), since the loss of E-cadherin expression has been demonstrated to increase cancer metastasis progresses (13,14,31), and tumor cells with increased expression of MTA1 indicate more invasive phenotypes (32).…”

Section: Loss Of E-cadherin Promotes Prostate Cancer Metastasis Via Usupporting

confidence: 50%

Loss of E-cadherin promotes prostate cancer metastasis via upregulation of metastasis-associated gene 1 expression

et al. 2012

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Abstract. E-cadherin is a key cell-to-cell adhesion molecule associated with the invasion and metastasis of tumor cells; however, the molecular mechanisms are not entirely understood. In this study, we investigated whether downregulation of E-cadherin by E-cadherin-specific small intefering RNA (siRNA) was able to promote malignant phenotypes of prostate cancer cells through upregulating the metastasis-associated gene 1 (MTA1) in vitro. The expression levels of E-cadherin in human paired prostate adenocarcinoma cell lines, PC-3M-2B4 (2B4) and PC-3M-1E8 (1E8), were investigated using western blot analysis. The alteration of malignant phenotypes associated with decreasing E-cadherin expression were assessed in 2B4 cells using wound-healing assays, solid-phase adhesion assays, invasion assays and cytoskeletal staining. The expression of E-cadherin and MTA1 in normal, localized and metastatic prostate cancer cells was analyzed using immunohistochemistry. Downregulation of E-cadherin using an RNA interference approach led to the upregulation of MTA1 expression, decreased tumor cell adhesion ability as well as enhanced cell mobility, invasion and cellular polarity compared with the controls (P<0.05). E-cadherin regulated MTA1 in a time-dependent manner. The correlation between E-cadherin and MTA1 was inversed in the prostate cancer group (P<0.05; r s =-0.434). The data suggest that E-cadherin plays an important role in prostate cancer metastasis, which is likely to be due to the regulation of MTA1 expression. E-cadherin may combine with MTA1 and alter the malignant phenotype of prostate cancer cells. A combined testing strategy for detecting MTA1 and E-cadherin may be sufficient for selecting high-risk patients with metastasis. Therefore, E-cadherin and MTA1 may be potential powerful factors for the treatment of various types of cancer.

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“…TGF-b is often overexpressed in tumor tissues including breast cancer, and facilitates cancer progression through a diverse repertoire of tumor-cell-autonomous and host-tumor interactions, including enhancement of cell motility and invasion, which involves the process of EMT. [26][27] When stimulated by 5 ng ml À 1 TGF-b1 for 24 h, breast cancer cells MDA-MB-231 and MDA-MB-435 undergo EMT by showing less uniform epithelial morphological changes, which were correlated with decreased E-cadherin expression and increased vimentin expression (Figures 4a and b). miRNAs are already known to be key regulators of the TGF-b pathway.…”

Section: Resultsmentioning

confidence: 99%

Critical role of miR-10b in transforming growth factor-β1-induced epithelial–mesenchymal transition in breast cancer

et al. 2014

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Epithelial-mesenchymal transition (EMT) is a key process in the tumor metastatic cascade that is characterized by the loss of cell-cell junctions and cell polarity, resulting in the acquisition of migratory and invasive properties. Recent evidence showed that altered microRNA-10b (miR-10b) expression was implicated in the occurrence of EMT of breast cancer. However, the exact role and underlying mechanisms of miR-10b in the EMT of breast cancer still remain unknown. In this study, miR-10b was found to be upregulated in breast cancer tissues and breast cancer cell lines and the expression of miR-10b was shown to be closely correlated with aggressiveness in breast cancer. Treating breast cancer cells with the miR-10b inhibitor increased E-cadherin expression while decreasing vimentin expression. At the same time, on inhibition of miR-10b, the invasion and proliferation ability of breast cancer cells also decreased. Transforming growth factor-b (TGF-b) is a multifunctional cytokine that induces EMT in multiple cell types. Here, we identified miR-10b as a target gene of TGF-b1. The expression of miR-10b increased during TGF-b1-induced EMT of breast cancer cells. Further study showed that inhibition of miR-10b expression partially reversed the EMT, invasion and proliferation induced by TGF-b1 in breast cancer cells. Taken together, these results demonstrated a novel function for miR-10b in TGF-b1-induced EMT in breast cancer and increased their metastatic potential. MiR-10b might become a possible target for gene therapy in breast cancer.Cancer Gene Therapy (2014) 21, 60-67; doi:10.1038/cgt.2013.82; published online 24 January 2014Keywords: miR-10b; TGF-b1; EMT; E-cadherin; invasion Breast cancer is one of the most common types of malignant cancers worldwide. Even though there has been considerable progress in the early detection and surgical therapy of breast cancer, there are B350 000 women who die from breast cancer each year. 1 The principal reason for mortality in breast cancer is invasion and metastasis rather than the primary cancer itself; therefore, there is an urgent need to understand the molecular mechanism and pathways that participate in the invasion and metastasis of breast cancer for better and improved treatment of women diagnosed with breast cancer. 2 Epithelial-mesenchymal transition (EMT) is a key step toward cancer metastasis, and E-cadherin is regarded as a main indicator of the epithelial-mesenchymal phenotype switching. 3 E-cadherin loss is suggestive of EMT, and tumor cell invasion and metastasis are associated with EMT. [4][5] EMT is triggered by many signaling pathways-for example, transforming growth factor-b (TGF-b), 6 fibroblast growth factor, 7 epidermal growth factor, 8 hepatocyte growth factor, 9 plateletderived growth factors 10 as well as different isoforms of Wnt proteins, 11 matrix metalloproteinases, 12 bone morphogenic proteins 13 and many others. Among these signaling pathways, TGF-b has been claimed to be critical for induction of the EMT phenotype, and TGF-b as a potent induc...

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RNA interference of metastasis‐associated gene 1 inhibits metastasis of B16F10 melanoma cells in a C57BL/6 mouse model

Cited by 33 publications

References 24 publications

MTA1 gene silencing inhibits invasion and alters the microRNA expression profile of human lung cancer cells

MTA1 gene silencing inhibits invasion and alters the microRNA expression profile of human lung cancer cells

Loss of E-cadherin promotes prostate cancer metastasis via upregulation of metastasis-associated gene 1 expression

Critical role of miR-10b in transforming growth factor-β1-induced epithelial–mesenchymal transition in breast cancer

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