MicroRNAs in breast cancer: oncogene and tumor suppressors with clinical potential

Wang, Wei; Luo, Yunping

doi:10.1631/jzus.b1400184

Cited by 148 publications

(123 citation statements)

References 147 publications

(95 reference statements)

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“…Our results were in agreement with other prior studies which reported that miR-21 over-expression was associated with tumor grades, higher proliferation index, and lymph node metastasis in BC [5,13,30,76]. Other previous studies showed that miR-21 levels are positively correlated with vascular invasion, visceral metastasis, and advanced clinical stage [13,46,77], and associated with poor response to therapy, and worse survival in BC [49,[78][79][80][81]. Moreover, miR-21 deregulation represented a global cancer phenomenon; associated with poor prognosis and survival in other cancer types including lung cancer [42,82], colorectal carcinoma [54,83], gastric cancer [84], pancreatic cancer [33], diffuse large B-cell lymphoma [36,37].…”

Section: Discussionsupporting

confidence: 92%

Pilot Study of Serum MicroRNA-21 as a Diagnostic and Prognostic Biomarker in Egyptian Breast Cancer Patients

et al. 2015

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Section: Discussionsupporting

confidence: 92%

Pilot Study of Serum MicroRNA-21 as a Diagnostic and Prognostic Biomarker in Egyptian Breast Cancer Patients

et al. 2015

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“…The expression of genes is regulated, in part, by microRNAs (miRNAs), endogenous small non-coding RNAs (ncRNAs), which play regulatory roles in normal cell function and in diseases, especially cancers, by predominantly binding to cis-elements in the 3′ untranslated region of specific mRNAs and regulating their translation or stability [9–13]. Recent studies have begun to elucidate the role of miRNAs in various biological processes, including adipocyte differentiation, metabolic integration, insulin resistance and appetite regulation [14–17].…”

Section: Introductionmentioning

confidence: 99%

Leptin and insulin up-regulate miR-4443 to suppress NCOA1 and TRAF4, and decrease the invasiveness of human colon cancer cells

Meerson

Yehuda

2016

BMC Cancer

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BackgroundObesity is a risk factor for colorectal cancer (CRC). Normal and tumor cells respond to metabolic hormones, such as leptin and insulin. Thus, obesity-associated resistance to these hormones likely leads to changes in gene expression and behavior of tumor cells. However, the mechanisms affected by leptin and insulin signaling in CRC cells remain mostly unknown.MethodsWe hypothesized that microRNAs (miRNAs) are involved in the regulation of tumorigenesis-related gene expression in CRC cells by leptin and insulin. To test this hypothesis, miRNA levels in the CRC-derived cell lines HCT-116, HT-29 and DLD-1 were profiled, following leptin and insulin treatment. Candidate miRNAs were validated by RT-qPCR. Predicted miRNA targets with known roles in cancer, were validated by immunoblots and reporter assays in HCT-116 cells. Transfection of HCT-116 cells with candidate miRNA mimic was used to test in vitro effects on proliferation and invasion.ResultsOf ~800 miRNAs profiled, miR-4443 was consistently up-regulated by leptin and insulin in HCT-116 and HT-29, but not in DLD-1, which lacked normal leptin receptor expression. Dose response experiments showed that leptin at 100 ng/ml consistently up-regulated miR-4443 in HCT-116 cells, concomitantly with a significant decrease in cell invasion ability. Transfection with miR-4443 mimic decreased invasion and proliferation of HCT-116 cells. Moreover, leptin and miR-4443 transfection significantly down-regulated endogenous NCOA1 and TRAF4, both predicted targets of miR-4443 with known roles in cancer metastasis. miR-4443 was found to directly regulate TRAF4 and NCOA1, as validated by a reporter assay. The up-regulation of miR-4443 by leptin or insulin was attenuated by the inhibition of MEK1/2.ConclusionsOur findings suggest that miR-4443 acts in a tumor-suppressive manner by down-regulating TRAF4 and NCOA1 downstream of MEK-C/EBP-mediated leptin and insulin signaling, and that insulin and/or leptin resistance (e.g. in obesity) may suppress this pathway and increase the risk of metastatic CRC.Electronic supplementary materialThe online version of this article (doi:10.1186/s12885-016-2938-1) contains supplementary material, which is available to authorized users.

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“…Collectively, the results of the present study demonstrate that miR-106b induces EMT via suppressing the expression of PTEN. Discussion miRNAs, small non-coding RNAs of ~22 nucleotides in length, have been demonstrated to be associated with the occurrence and development of human cancer types where they may function as tumor suppressors or oncogenes (3)(4)(5)(6)20,21). Previous studies have demonstrated the abnormal expression of a number of types of miRNAs in ESCC (22,23).…”

Section: Downregulation Of Pten Partially Increased the Invasion Metmentioning

confidence: 97%

miR-106b promotes cell invasion and metastasis via PTEN mediated EMT in ESCC

et al. 2018

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Abstract. MicroRNA (miR)-106b serves an essential function in a variety of human cancer types, particularly in the process of invasion and metastasis. However, the function and mechanism of miR-106b in the invasion and metastasis of esophageal squamous cell carcinoma (ESCC) has remained elusive. In the present study, it was demonstrated that miR-106b was upregulated in ESCC tissues and cell lines. Furthermore, miR-106b expression in ESCC tissues was positively associated with lymphatic metastasis. Inhibition of miR-106b in EC-1 and EC9706 cells decreased not only the invasion and metastasis ability but also the proliferation ability of EC-1 and EC9706 cells. In addition, miR-106b had the ability to induce epithelial-to-mesenchymal transition (EMT) in EC-1 and EC9706 cells. In terms of the underlying mechanism, it was revealed that miR-106b promoted the invasion, metastasis and proliferation ability of EC-1 and EC9706 cells by directly targeting phosphatase and tension homolog (PTEN). Furthermore, miR-106b induced EMT in EC-1 and EC9706 cells by suppressing the expression of PTEN. In summary, the present study revealed that miR-106b contributed to invasion and metastasis in ESCC by regulating PTEN mediated EMT. Downregulation of miR-106b may be a novel strategy for preventing tumor invasion and metastasis. IntroductionEsophageal squamous cell carcinoma (ESCC) is the most malignant lesion in China, particularly in Linzhou, Henan (1).Treatment of ESCC is largely useless due to the occurrence of invasion and metastasis in the early stage. However, the mechanism of invasion and metastasis of ESCC has been poorly elucidated (2).Epithelial-to-mesenchymal transition (EMT) now is always viewed as a key event that occurs during cancer invasion and metastasis. However, current understanding of the alterations that give rise to the occurrence of EMT is limited. MicroRNAs (miRNA/miRs) are small non-coding RNA molecules that may directly regulate target gene expression by binding to their 3'-untranslated regions (3'-UTRs) (3,4). Furthermore, miRNAs have been demonstrated to serve notable functions in tumor invasion and metastasis by functioning as EMT suppressors or inducers (5,6). miR-106b is a type of miRNA transcribed from the miR-106b-25 cluster located on chromosome 7 (7). Yau et al (8) reported that miR-106b overexpressed in hepatocellular carcinoma cells and that the overexpression of miR-106b may promote cell migration and metastasis by activating the EMT process. Zhou et al (9) additionally demonstrated that miR-106b contributed as an EMT inducer in breast cancer. However, whether miR-106b participates in the invasion and metastasis process of ESCC by inducing EMT and the mechanism of how miR-106b induces EMT in ESCC had not been fully explored until now. miRNAs participate in the occurrence and development of a cancer by regulating the post-transcriptional process of their target gene. Several genes have been verified to be the targets of miR-106b, including transforming growth factor-β type II receptor, cyclin de...

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MicroRNAs in breast cancer: oncogene and tumor suppressors with clinical potential

Cited by 148 publications

References 147 publications

Pilot Study of Serum MicroRNA-21 as a Diagnostic and Prognostic Biomarker in Egyptian Breast Cancer Patients

Pilot Study of Serum MicroRNA-21 as a Diagnostic and Prognostic Biomarker in Egyptian Breast Cancer Patients

Leptin and insulin up-regulate miR-4443 to suppress NCOA1 and TRAF4, and decrease the invasiveness of human colon cancer cells

miR-106b promotes cell invasion and metastasis via PTEN mediated EMT in ESCC

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