miR-92a family and their target genes in tumorigenesis and metastasis

Li, Molin; Guan, Xingfang; Sun, Yuqiang; Mi, Jun; Shu, Xiaohong; Liu, Fang; Li, Chuangang

doi:10.1016/j.yexcr.2013.12.025

Cited by 99 publications

(82 citation statements)

References 59 publications

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“…In the past several years, more and more miRNAs have been confirmed as modulators of cell proliferation, apoptosis, and therapy resistance in lung cancer [14,15]. Among them, miR-92a attracts much attention because it can regulate tumor progression in a variety of cancers as an oncogenic or a tumorsuppressive miRNA [16][17][18][19][20][21]. Although, recently, a study has been demonstrated that miR-92a mediates STAT3-induced MMP activity and invasiveness by inhibiting RECK in lung cancer [22], the detail function especially in regard to response to chemotherapy and underlying molecular mechanism of miR-92a in NSCLC have not been totally elucidated.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-92a promotes growth, metastasis, and chemoresistance in non-small cell lung cancer cells by targeting PTEN

et al. 2015

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MicroRNA-92a (miR-92a) has been reported to play important roles in tumorigenesis of human various cancers. However, the roles and underlying molecular mechanism of miR-92a in non-small cell lung cancer (NSCLC) have not been totally elucidated. Therefore, the aims of this study were to determine the role of miR-92a and to elucidate its regulatory mechanism in NSCLC. We found that miR-92a was significantly upregulated in NSCLC tissues compared to matched adjacent normal lung tissues, and its expression is significantly associated with clinical characteristics of patients, including tumor, node, and metastasis (TNM) stage; tumor size; and lymph node metastasis (all P < 0.01). Function assays demonstrated that upregulation of miR-92a in NSCLC cells promoted cell proliferation, migration, and invasion, decreased apoptosis and caspase-3 activity, and enhanced chemoresistance of NSCLC cells, whereas downregulation of miR-92a showed the opposite effects. Moreover, phosphatase and tensin homolog (PTEN), a unique tumor suppressor gene, was confirmed as a direct target of miR-92a, and PTEN messenger RNA (mRNA) expression was decreased in NSCLC tissues and was inversely correlated with miR-92a. Downregulation of PTEN could mimic the same effects of miR-92a mimic in NSCLC cells and rescue the effects on NSCLC cells induced by miR-92a inhibitor. Taken together, these findings suggested that miR-92a could promote growth, metastasis, and chemoresistance in NSCLC cells at least partially by targeting PTEN.

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Section: Introductionmentioning

confidence: 99%

MicroRNA-92a promotes growth, metastasis, and chemoresistance in non-small cell lung cancer cells by targeting PTEN

et al. 2015

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“…miR-486 -5p (75), miR-1266 (76) or miR-218 (77). Furthermore, we identified oncogenic factors among the down-regulated miRNAs, such as miR-25 and miR-92a (78) and the miRNA family miR-221/222, which is known to promote EMT (79).…”

Section: P53-mediated Regulationsmentioning

confidence: 99%

p53-Regulated Networks of Protein, mRNA, miRNA, and lncRNA Expression Revealed by Integrated Pulsed Stable Isotope Labeling With Amino Acids in Cell Culture (pSILAC) and Next Generation Sequencing (NGS) Analyses

Hünten

Kaller

Drepper

et al. 2015

Molecular & Cellular Proteomics

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We determined the effect of p53 activation on de novo protein synthesis using quantitative proteomics (pulsed stable isotope labeling with amino acids in cell culture/ pSILAC) in the colorectal cancer cell line SW480. This was combined with mRNA and noncoding RNA expression analyses by next generation sequencing (RNA-, miR-Seq). The p53 gene encodes a tumor-suppressive protein, which is activated by DNA damage, but also by other types of cellular stress (1). p53 functions as a transcription factor that regulates the expression of numerous genes, which mediate cell cycle arrest, senescence and apoptosis, or suppress epithelial-mesenchymal-transition (EMT) 1 and metastasis (2-4). p53 is mutated in at least 50% of human cancers with From the ‡Experimental and Molecular Pathology, Institute of Pathology,

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“…It has been suggested that miRNAs are predicted to regulate 30% of human genes (Carthew, 2006). Many studies have identified that miRNAs are potent drivers of various biological processes, including cell proliferation, cell differentiation, apoptosis and tumorigenesis (Zamore and Haley, 2005;Li et al, 2014;Tufekci et al, 2014). Recent emerging evidences have suggested that differential expression of miRNAs was related to various human cancers development and progression by regulating the expression of tumor suppressor genes or proto-oncogenes (Cui et al, 2014;Donadelli et al, 2014;Gu et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

Association between the DICER rs1057035 Polymorphism and Cancer Risk: Evidence from a Meta-analysis of 1,2675 Individuals

Yu¹,

Kuang²,

Yin³

2015

Asian Pacific Journal of Cancer Prevention

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Background: DICER, one of the microRNA (miRNA) biogenesis proteins, is involved in the maturation of miRNAs and is implicated in cancer development and progression. The results from previous epidemiological studies on associations between DICER rs1057035 polymorphism and cancer risk were inconsistent. Thereforewe performed this meta-analysis to summarize possible associations. Materials and Methods: We searched all relevant articles on associations between DICER rs1057035 polymorphism and cancer risk from PubMed, EMBASE, Chinese Biomedical Literature and Chinese National Knowledge Infrastructure until August 2014. Odds ratios (ORs) with 95% confidence intervals (CIs) were calculated to assess any associations. Heterogeneity tests, sensitivity analyses and publication bias assessments were also performed in this meta-analysis. All analyses were conducted using STATA software. Results: Seven case-control studies, including 4,875 cancer cases and 7,800 controls were included in the meta-analysis. Overall, the results indicated that the C allele of DICER rs1057035 polymorphism was significantly associated with decreased cancer risk in allelic comparison, heterozygote and dominant genetic models (C vs T: OR=0.88, 95%CI 0.81-0.95, p=0.002; TC vs TT: OR=0.85, 95%CI 0.77-0.93, p=0.001; CC/TC vs TT: OR=0.86, 95%CI 0.78-0.94, p=0.001). In the subgroup analysis by ethnicity, a significantly decreased cancer risk was found in Asian but not Caucasian populations. Conclusions: The present meta-analysis suggests that the C allele of the DICER rs1057035 polymorphism probably decreases cancer risk. However, this association may be Asian-specific and the results should be treated with caution. Further well-designed studies based on larger sample sizes and group of populations are needed to validate these findings.

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miR-92a family and their target genes in tumorigenesis and metastasis

Cited by 99 publications

References 59 publications

MicroRNA-92a promotes growth, metastasis, and chemoresistance in non-small cell lung cancer cells by targeting PTEN

MicroRNA-92a promotes growth, metastasis, and chemoresistance in non-small cell lung cancer cells by targeting PTEN

p53-Regulated Networks of Protein, mRNA, miRNA, and lncRNA Expression Revealed by Integrated Pulsed Stable Isotope Labeling With Amino Acids in Cell Culture (pSILAC) and Next Generation Sequencing (NGS) Analyses

Association between the DICER rs1057035 Polymorphism and Cancer Risk: Evidence from a Meta-analysis of 1,2675 Individuals

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