MicroRNA-27a functions as an oncogene in gastric adenocarcinoma by targeting prohibitin

Liu, Tao; Tang, Hua; Lang, Yuanyuan; Liu, Min; Li, Xin

doi:10.1016/j.canlet.2008.08.003

Cited by 313 publications

(265 citation statements)

References 31 publications

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“…The functional implications of miR-125b in GC tumorigenesis remained to be addressed. Our tissue analysis indicated underexpression of miR-27a in GC; this miRNA has been found oncogenic to GC cells by targeting prohibitin (Liu et al, 2009). This contradiction requires further clarification.…”

Section: Discussionmentioning

confidence: 76%

Overexpression of miR-370 and downregulation of its novel target TGFβ-RII contribute to the progression of gastric carcinoma

et al. 2011

Oncogene

101

100

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MicroRNAs (miRNAs) are endogenous non-coding RNAs that are known to be involved in the pathogenesis of tumors. Gastric carcinoma (GC) is a common malignancy worldwide. The aim of this study was the identification of the expression signature and functional roles of aberrant miRNAs in GC. Initial screening established a profile of aberrantly expressed miRNAs in tumors. miR-370 was confirmed to be overexpressed in GC tissues. Higher expression of miR-370 in GC tissues was associated with more advanced nodal metastasis and a higher clinical stage compared with controls. In addition, significantly higher level of miR-370 was noted in the plasma of GC patients compared with controls. Patients having more invasive or advanced tumors also exhibited a higher plasma level of miR-370. In vitro assays indicated that exogenous miR-370 expression enhanced the oncogenic potential of GC cells. The AGS-GFPM2 cells with exogenous miR-370 expression also exhibited enhanced abdominal metastatic dissemination in nude mice. Reporter assays confirmed that miR-370 targeted predicted sites in 3 0 UTR of transforming growth factor-b receptor II (TGFb-RII) gene. The exogenous miR-370 expression decreased TGFb-RII expression and the phosphorylation of Smad3 elicited by TGFb1. The TGFb1-mediated repression in cell migration was reverted by exogenous miR-370 expression. A reverse correlation between miR-370 and TGFb-RII expression was noted in GC tissues. This study concludes that miR-370 is a miRNA that is associated with GC progression by downregulating TGFb-RII. The miRNA expression profile described in this study should contribute to future studies on the role of miRNAs in GC.

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Section: Discussionmentioning

confidence: 76%

Overexpression of miR-370 and downregulation of its novel target TGFβ-RII contribute to the progression of gastric carcinoma

et al. 2011

Oncogene

101

100

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“…Thus, the percentage of cells in G 2 -M was consequently increased. Other studies also found that the suppression of miR-27a can inhibit gastric cancer cell growth [57] and overexpression of miR-27a increases the fat accumulation and cell proliferation of Hepatic stellate cells [58]. Therefore, miR-27a is considered as an oncogene.…”

Section: Discussionmentioning

confidence: 95%

A genetic variant in the pre-miR-27a oncogene is associated with a reduced familial breast cancer risk

Yang

Schlehe

Hemminki

et al. 2009

Breast Cancer Res Treat

113

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International audienceMicroRNAs (miRNAs) regulate pathways involved in cell differentiation, proliferation, development, and apoptosis by degradation of target mRNAs and/or repression of their translation. Although the single nucleotide polymorphisms (SNPs) in miRNAs target sites have been studied, the effects of SNPs in miRNAs are largely unknown. In our study, we first systematically sequenced miRNA genes reported to be involved in breast cancer to identify/verify SNPs. We analyzed four SNPs, one located in the pre-miRNA and the other three located in miRNA flanking regions, for a putative association with breast cancer risk. The SNP rs895819, located in the terminal loop of pre-miRNA-27a, showed a protective effect. In a large familial breast cancer study cohort, the rare [G] allele of rs895819 was found to be less frequent in the cases than in the controls, indicating a reduced familial breast cancer risk ([G] vs. [A]: OR = 0.88, 95% CI 0.78-0.99, = 0.0287). Furthermore, age stratification revealed that the protective effect was mainly observed in the age group < 50 years of age ([G] vs. [A]: OR = 0.83, 95% CI 0.70-0.98, = 0.0314), whereas no significant effect was observed in the age group ≥ 50 years of age, indicating a possible hormone-related effect. It has been shown that artificial mutations in the terminal loop of miR-27a can block the maturation process of the miRNA. We hypothesize that the G-variant of rs895819 might impair the maturation of the oncogenic miR-27a and thus, is associated with familial breast cancer risk

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“…These programs suggested a great number of genes as possible targets of miR-27a. Among the predicted targets, several genes including FOXO1 (forkhead box O1), Myt-1 (myelin transcription factor 1), prohibitin, sprouty2 and ZBTB10 (zinc finger and BTB domain containing 10) have been previously identified as the targets of miR-27a (Mertens-Talcott et al, 2007;Guttilla and White, 2009;Liu et al, 2009;Ma et al, 2010). We focused on genes meeting the following criteria: (1) cancer suppressor genes; (2) ability to bind miR-27a (the free energy (Mfe) of binding of the target gene's mRNA with miR-27a oÀ13.4 kcal/mol (Zhao et al, 2007)); and (3) genes that function in the regulation of cell proliferation.…”

Section: The Fbxw7 Gene Is a Direct Target Of Mir-27amentioning

confidence: 99%

Upregulation of miR-27a contributes to the malignant transformation of human bronchial epithelial cells induced by SV40 small T antigen

Wang

et al. 2011

Oncogene

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MicroRNA-27a functions as an oncogene in gastric adenocarcinoma by targeting prohibitin

Cited by 313 publications

References 31 publications

Overexpression of miR-370 and downregulation of its novel target TGFβ-RII contribute to the progression of gastric carcinoma

Overexpression of miR-370 and downregulation of its novel target TGFβ-RII contribute to the progression of gastric carcinoma

A genetic variant in the pre-miR-27a oncogene is associated with a reduced familial breast cancer risk

Upregulation of miR-27a contributes to the malignant transformation of human bronchial epithelial cells induced by SV40 small T antigen

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