MiR-572 prompted cell proliferation of human ovarian cancer cells by suppressing PPP2R2C expression

Wu, Aihua; Huang, Yingna; Zhang, Lanzhen; Tian, Geng; Liao, Qiong-Zhi; Chen, Shiling

doi:10.1016/j.biopha.2015.12.005

Cited by 33 publications

(29 citation statements)

References 20 publications

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“…For example, miR-367 exerts oncogenic effects in osteosarcoma and promotes the proliferation, migration and invasion of tumor cells with the regulation of DOC-2/DAB2 interactive protein, which was consistent with the oncogenic role of miR-367 in RCC (12,13). miR-572 is a type of miR that was recently confirmed to be involved in various types of cancer, including chronic lymphocytic leukemia (14), nasopharyngeal carcinoma (15), ovarian cancer (16) and basal cell carcinoma (17). Results from a study by Wang et al (18) revealed that, compared with corresponding non-tumor controls, miR-572 was markedly elevated in the serum of patients with RCC.…”

Section: Microrna-572 Functions As An Oncogene and A Potential Biomarsupporting

confidence: 66%

microRNA‑572 functions as an oncogene and a potential biomarker for renal cell carcinoma prognosis

Pan

Zhao

et al. 2018

Oncol Rep

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Renal cell carcinoma (RCC) is the third most common urological malignancy in the USA and represents 2‑3% of all adult malignancies. Furthermore, the incidence of RCC has been progressively increasing over recent years. Although the morbidity of treatment has decreased with the use of multidisciplinary synthetic therapy, the prognosis of terminal cancer remains poor, with a 5‑year survival rate of 5‑10%. MicroRNAs (miRs) have been correlated with the regulation of 30‑60% of the protein-coding genes and act as oncogenes or anti‑oncogenes in RCC. Considering this research, miRNAs are likely to be the biomarkers for tumor diagnosis, prognosis and the targets for RCC management. In the present study, 42 formalin‑fixed paraffin‑embedded RCC samples were used. The expression of miR‑572 and the role of miR‑572 in RCC cell proliferation, migration and apoptosis was determined by performing reverse transcription‑quantitative polymerase chain reaction analysis, wound scratch assays, cell proliferation assays, Transwell assays and flow cytometry assays, respectively. Further experiments were conducted to clarify the correlation between miR‑572 expression and clinicopathological variables or overall survival. Furthermore, the expression levels of miR‑572 were evaluated for the prognosis value of patients with RCC. Upregulation of miR‑572 was observed in RCC tissues and RCC cell lines. miR‑572 promoted 786‑O and ACHN cell proliferation and mobility and inhibited early apoptosis. In Cox proportional hazard regression analyses, results of the univariate and multivariate analysis indicated that the patients with low miR‑572 expression had a significantly longer overall survival compared with the patients with high miR‑572 expression (univariate analysis, P=0.037; multivariate analysis, P=0.034). Results of the Kaplan‑Meier survival curves revealed that the patients with downregulated miR‑572 have a significantly longer overall survival compared with the patients with highly expressed miR‑572 (P=0.019). To conclude, the results of the present study suggest that tumor oncogene miR‑572 is a potential biomarker for the diagnosis, treatment and prognosis for RCC.

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Section: Microrna-572 Functions As An Oncogene and A Potential Biomarsupporting

confidence: 66%

microRNA‑572 functions as an oncogene and a potential biomarker for renal cell carcinoma prognosis

Pan

Zhao

et al. 2018

Oncol Rep

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“…PPP2R2C is another interesting gene downregulated in EAC, with simultaneous copy number loss and hypermethylation (Supplementary Table S2). Dysfunction of PPP2R2C through microRNAs has been recently reported in some human cancers108109. Our results indicate that dysfunction of these genes by both genetic and epigenetic interaction mechanisms may play an important role in Barrett’s tumourigenesis and EAC.…”

Section: Resultssupporting

confidence: 68%

Integrated molecular analysis reveals complex interactions between genomic and epigenomic alterations in esophageal adenocarcinomas

Peng

Guo

Chen

et al. 2017

Sci Rep

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The incidence of esophageal adenocarcinoma (EAC) is rapidly rising in the United States and Western countries. In this study, we carried out an integrative molecular analysis to identify interactions between genomic and epigenomic alterations in regulating gene expression networks in EAC. We detected significant alterations in DNA copy numbers (CN), gene expression levels, and DNA methylation profiles. The integrative analysis demonstrated that altered expression of 1,755 genes was associated with changes in CN or methylation. We found that expression alterations in 84 genes were associated with changes in both CN and methylation. These data suggest a strong interaction between genetic and epigenetic events to modulate gene expression in EAC. Of note, bioinformatics analysis detected a prominent K-RAS signature and predicted activation of several important transcription factor networks, including β-catenin, MYB, TWIST1, SOX7, GATA3 and GATA6. Notably, we detected hypomethylation and overexpression of several pro-inflammatory genes such as COX2, IL8 and IL23R, suggesting an important role of epigenetic regulation of these genes in the inflammatory cascade associated with EAC. In summary, this integrative analysis demonstrates a complex interaction between genetic and epigenetic mechanisms providing several novel insights for our understanding of molecular events in EAC.

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“…In total, there were 6847 increased and 3219 decreased regions ( Figure S5A). PPP2R2C, a tumor suppressor gene [41], exhibited elevated H3K4me3 signals with ICG-001 treatment compared to the control. In contrast, NKIRAS1, encoding a RAS-like protein, exhibited a decreased H3K4me3 signal with ICG-001 treatment ( Figure S5B).…”

Section: Histone Acetyltransferase Inhibitors Alter Global H3k27ac Anmentioning

confidence: 95%

Disruption of Broad Epigenetic Domains in PDAC Cells by HAT Inhibitors

et al. 2019

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The spreading of epigenetic domains has emerged as a distinguishing epigenomic phenotype for diverse cell types. In particular, clusters of H3K27ac- and H3K4me3-marked elements, referred to as super-enhancers, and broad H3K4me3 domains, respectively, have been linked to cell identity and disease states. Here, we characterized the broad domains from different pancreatic ductal adenocarcinoma (PDAC) cell lines that represent distinct histological grades. Our integrative genomic analysis found that human derived cell line models for distinct PDAC grades exhibit characteristic broad epigenetic features associated with gene expression patterns that are predictive of patient prognosis and provide insight into pancreatic cancer cell identity. In particular, we find that genes marked by overlapping Low-Grade broad domains correspond to an epithelial phenotype and hold potential as markers for patient stratification. We further utilize ChIP-seq to compare the effects of histone acetyltransferase (HAT) inhibitors to detect global changes in histone acetylation and methylation levels. We found that HAT inhibitors impact certain broad domains of pancreatic cancer cells. Overall, our results reveal potential roles for broad domains in cells from distinct PDAC grades and demonstrate the plasticity of particular broad epigenomic domains to epigenetic inhibitors.

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MiR-572 prompted cell proliferation of human ovarian cancer cells by suppressing PPP2R2C expression

Cited by 33 publications

References 20 publications

microRNA‑572 functions as an oncogene and a potential biomarker for renal cell carcinoma prognosis

microRNA‑572 functions as an oncogene and a potential biomarker for renal cell carcinoma prognosis

Integrated molecular analysis reveals complex interactions between genomic and epigenomic alterations in esophageal adenocarcinomas

Disruption of Broad Epigenetic Domains in PDAC Cells by HAT Inhibitors

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