The Role of MicroRNAs in Breast Cancer Migration, Invasion and Metastasis

Tang, Joy; Ahmad, Aamir; Sarkar, Fazlul H.

doi:10.3390/ijms131013414

Cited by 158 publications

(145 citation statements)

References 125 publications

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“…Recently, the abnormal expression of miRNAs in several types of cancer has been confirmed, including colon cancer, hepatocellular carcinoma, lung cancer and breast cancer (5)(6)(7)(8). Emerging evidence has indicated that miRNAs function as oncogenes or tumor suppressor genes to control cell proliferation, invasion, migration, differentiation and apoptosis (9)(10)(11). For example, miR-638 has been shown to inhibit cell proliferation and invasion and to regulate the cell cycle by targeting tetraspanin 1 (12).…”

Section: Introductionmentioning

confidence: 99%

microRNA-214 enhances the invasion ability of breast cancer cells by targeting p53

Wang

et al. 2015

International Journal of Molecular Medicine

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Abstract. Breast cancer (BC) is the foremost cause of cancerrelated mortality in women worldwide. An increasing number of studies has confirmed that microRNAs (miRNAs or miRs) play an important role in the development and progression of BC. microRNA-214 (miR-214), a member of the miRNA family, has been demonstrated to function as both a tumor suppressor and oncogene in various types of human cancer. However, the biological function of miR-214 in BC remains unclear. The present study was designed to investigate the potential role of miR-214 in the development and progression of BC. Our results revealed that miR-214 expression was significantly increased in the BC tissues compared with the adjacent benign tissues, and that the upregulation of miR-214 was significantly associated with the invasion ability of the BC cells. Furthermore, p53, which has been reported to be downregulated in BC, was predicted to be the target gene of miR-214 using bioinformatics software programs. Moreover, luciferase reporter vectors were constructed and it was confirmed that p53 is a target of miR-214. Following the transfection of miR-214 into BC cells, we found that the overexpression of miR-214 markedly enhanced cell invasion through the downregulation of p53 expression. By contrast, the overexpression of p53 abrogated the effects of miR-214. In conclusion, this study demonstrates that miR-214 functions as an oncogene in BC, at least partly by promoting cell invasion through the downregulation of p53. Therefore, miR-214 may be a potential therapeutic target for the treatment of BC.

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Section: Introductionmentioning

confidence: 99%

microRNA-214 enhances the invasion ability of breast cancer cells by targeting p53

Wang

et al. 2015

International Journal of Molecular Medicine

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“…Carcinogenic miRNAs are often overexpressed in tumors and are termed "oncogenic" because they play similar roles as oncogenes during the process of cancer development. In addition, the expression of tumor suppressing miRNAs is often downregulated in tumors; these miRNAs are called tumor suppressor miRNAs because they function similarly to tumor suppressor genes (Tang et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

miR-153 Silencing Induces Apoptosis in the MDA-MB-231 Breast Cancer Cell Line

Anaya-Ruı́z

Cebada²,

Delgado-López³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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MicroRNAs (miRNAs) are small, non-coding RNAs (18-25 nucleotides) that post-transcriptionally modulate gene expression by negatively regulating the stability or translational efficiency of their target mRNAs. In this context, the present study aimed to evaluate the in vitro effects of miR-153 inhibition in the breast carcinoma cell line MDA-MB-231. Forty-eight hours after MDA-MB-231 cells were transfected with the miR-153 inhibitor, an MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay was utilized to determine the effects of miR-153 on cell viability. Flow cytometry analysis and assessment of caspase 3/7 activity were adopted to determine whether miR-153 affects the proliferation rates and apoptosis levels of MDA-MB-231 cells. Our results showed that silencing of miR-153 significantly inhibited growth when compared to controls at 48 hours, reducing proliferation by 37.6%, and inducing apoptosis. Further studies are necessary to corroborate our findings and examine the potential use of this microRNA in future diagnostic and therapeutic interventions.

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“…miRNAs regulate signaling pathways at the post‐transcriptional level and are frequently deregulated in breast cancer. It has been shown that aberrantly expressed miRNAs promote cancer development, metastasis formation, and potently induce drug resistance in both tumor cells and cells of the tumor microenvironment (Bott et al ., 2017; Breunig et al ., 2017; Dvinge et al ., 2013; Tang et al ., 2012; Zhu et al ., 2011). In a previous study, we have identified a tumor‐suppressive function of the miR‐520/miR373 family by targeting TGFBR2 in breast cancer cells (Keklikoglou et al ., 2012).…”

Section: Introductionmentioning

confidence: 99%

TGFβ1 regulates HGF‐induced cell migration and hepatocyte growth factor receptor MET expression via C‐ets‐1 and miR‐128‐3p in basal‐like breast cancer

et al. 2018

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Breast cancer is the most common cancer in women worldwide. The tumor microenvironment contributes to tumor progression by inducing cell dissemination from the primary tumor and metastasis. TGFβ signaling is involved in breast cancer progression and is specifically elevated during metastatic transformation in aggressive breast cancer. In this study, we performed genomewide correlation analysis of TGFBR2 expression in a panel of 51 breast cancer cell lines and identified that MET is coregulated with TGFBR2. This correlation was confirmed at the protein level in breast cancer cell lines and human tumor tissues. Flow cytometric analysis of luminal and basal‐like breast cancer cell lines and examination of 801 tumor specimens from a prospective cohort of breast cancer patients using reverse phase protein arrays revealed that expression of TGFBR2 and MET is increased in basal‐like breast cancer cell lines, as well as in triple‐negative breast cancer tumor tissues, compared to other subtypes. Using real‐time cell analysis technology, we demonstrated that TGFβ1 triggered hepatocyte growth factor (HGF)‐induced and MET‐dependent migration in vitro. Bioinformatic analysis predicted that TGFβ1 induces expression of C‐ets‐1 as a candidate transcription factor regulating MET expression. Indeed, TGFβ1‐induced expression of ETS1 and breast cancer cell migration was blocked by knockdown of ETS1. Further, we identified that MET is a direct target of miR‐128‐3p and that this miRNA is negatively regulated by TGFβ1. Overexpression of miR‐128‐3p reduced MET expression and abrogated HGF‐induced cell migration of invasive breast cancer cells. In conclusion, we have identified that TGFβ1 regulates HGF‐induced and MET‐mediated cell migration, through positive regulation of C‐ets‐1 and negative regulation of miR‐128‐3p expression in basal‐like breast cancer cell lines and in triple‐negative breast cancer tissue.

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The Role of MicroRNAs in Breast Cancer Migration, Invasion and Metastasis

Cited by 158 publications

References 125 publications

microRNA-214 enhances the invasion ability of breast cancer cells by targeting p53

microRNA-214 enhances the invasion ability of breast cancer cells by targeting p53

miR-153 Silencing Induces Apoptosis in the MDA-MB-231 Breast Cancer Cell Line

TGFβ1 regulates HGF‐induced cell migration and hepatocyte growth factor receptor MET expression via C‐ets‐1 and miR‐128‐3p in basal‐like breast cancer

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