Alterations of MicroRNAs Contribute to Colon Carcinogenesis

Schetter, Aaron J.; Harris, Curtis C.

doi:10.1053/j.seminoncol.2011.08.009

Cited by 72 publications

(60 citation statements)

References 73 publications

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“…microRNAs, a newly discovered class of non-coding small RNAs, have been recognized as potential targets for tumor treatment due to their important roles in carcinogenesis and cancer progression via binding to specific complementary sites within the 3' untranslated regions (3'UTR) of their target gene mRNAs (16)(17)(18). Accumulated studies have shown that miRNAs may function as oncogenes or tumor suppressors in the tumorigenesis of various human cancers depending on the cellular contexts and the target genes that they regulate.…”

Section: Introductionmentioning

confidence: 99%

miR-200a suppresses cell growth and migration by targeting MACC1 and predicts prognosis in hepatocellular carcinoma

et al. 2014

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Abstract. miR-200a suppresses tumor development and progression; however, its role in tumor growth and metastasis of hepatocellular carcinoma (HCC) and the underlying mechanism have not been elucidated. In the present study, we identified that miR-200a was markedly downregulated in HCC and exerted suppressive effects on tumor cell growth and metastasis. We identified that miR-200a suppressed tumor growth and metastasis by directly targeting MACC1. In addition, HCC patients with low miR-200a expression had significantly worse prognosis than those with high expression of miR-200a. These findings suggest that miR200a may be recognized as a novel potential biomarker to predict the survival of patients with HCCs following liver transplantation.

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Section: Introductionmentioning

confidence: 99%

miR-200a suppresses cell growth and migration by targeting MACC1 and predicts prognosis in hepatocellular carcinoma

et al. 2014

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“…Emerging evidence shows that miRNAs are involved in the biological processes related to apoptosis, proliferation, differentiation, invasion and metastasis, while its deregulation is crucial to cancer initiation and progression. [16][17][18][19] In an initial screen for miRNAs differentially expressed in human breast cancer cells, the three most significantly upregulated miRNAs, miR-155, miR-9 and microRNA-10b (miR-10b), were identified. 20 MiR-10b is a particularly interesting candidate given its close correlation with metastatic behaviors.…”

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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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“…Thus, variations in these sequences may result in significant functional consequences, making them ideal candidates for cancer risk prediction. Many have been validated as potential oncogenes or tumor suppressor genes in CRC, such as miR-143, miR-145, miR-21, and miR200c (Schetter and Harris, 2011). miRNA expression profile analyses indicate that these sequences play an etiological role in the initiation and progression of this condition.…”

Section: Differentially Expressed Mirnas In Crcmentioning

confidence: 99%

MicroRNA variants and colorectal cancer risk: a meta-analysis

Pan¹,

Xiao²,

Qin³

et al. 2016

Genet. Mol. Res.

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ABSTRACT. Colorectal cancer (CRC) is a multi-factorial disease, and genetic background may contribute to its etiology. Single nucleotide polymorphisms (SNPs) in microRNAs (miRNAs) may be used as specific markers of predisposition for CRC diagnosis and prevention. In this review, we summarize and discuss recent publications evaluating the roles of miRNA SNPs in CRC. A meta-analysis was also carried out to assess the association between the five most frequently studied miRNA SNPs and CRC risk. No relationship was established between this disease and the three SNPs rs11614913, rs2910164, and rs3746444 in miR-196a-2, miR-146a, and miR-499, respectively. However, polymorphisms of miR-149 (rs2292832; CT vs TT: odds ratio [OR] = 0.816, 95% confidence interval [CI] = 0.691-0.963; CC+CT vs TT: OR = 0.834, 95%CI = 0.715-0.972) and pre-miR-27a (rs895819; GG vs AA: OR = 1.534, 95%CI = 1.148-2.049; GG+AG vs AA: OR = 1.324, 95%CI = 1.066-1.645) were found to be associated with CRC in our analysis. In conclusion, the SNPs rs2292832 in miR-149 and rs895819 in pre-miR-27a were associated with CRC susceptibility, whereas rs11614913, rs2910164, and rs3746444 in miR-196a-2, miR-146a, and miR-499, respectively, were not. Further studies should be carried out to validate these findings.

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Alterations of MicroRNAs Contribute to Colon Carcinogenesis

Cited by 72 publications

References 73 publications

miR-200a suppresses cell growth and migration by targeting MACC1 and predicts prognosis in hepatocellular carcinoma

miR-200a suppresses cell growth and migration by targeting MACC1 and predicts prognosis in hepatocellular carcinoma

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

MicroRNA variants and colorectal cancer risk: a meta-analysis

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