MicroRNA-195: a review of its role in cancers

Yu, Wanpeng; Liang, Xiao; Li, Xiangdong; Zhang, Yuan; Sun, Zhenqiang; Liu, Ying; Wang, Jianxun

doi:10.2147/ott.s183600

Cited by 68 publications

(47 citation statements)

References 174 publications

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“…MicroRNAs are thought to be crucial in various physiological and pathological processes, especially in cancer [71][72][73][74][75]. MiR-195-59 has been previously studied in solid tumors [76][77][78]. In prostate cancer, miR-195 inhibits tumor progression [79,80].…”

Section: Discussionmentioning

confidence: 99%

Gene Expression Alterations and Molecular Analysis of CHEK1 in Solid Tumors

Fadaka

Bakare

Sibuyi

et al. 2020

Cancers

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Alterations in the Checkpoint kinase (CHEK1) gene, its regulation, and the possible clinical outcomes in human solid tumors have not been previously examined. Therefore, the present study was carried out to evaluate the expression of CHEK1 in solid tumors as well as the mechanism by which it can be regulated through non-coding RNAs. The expression of CHEK1 was investigated using Oncomine analysis. cBioPortal, Kaplan–Meier Plotter, and PrognoScan were performed to identify the prognostic roles of this gene in solid tumors. The copy number alteration, mutation, interactive analysis, and visualization of the altered networks were performed by cBioPortal. The molecular binding analysis was carried out by Schrodinger suite, PATCHDOCK, and discovery studio visualizer. The study demonstrated that the CHEK1 gene was differentially expressed in four different cancers, and that reduced CHEK1 mRNA expression is an unfavorable prognostic factor for patients with gastric and colorectal cancer. The molecular docking results showed that the CHEK1 gene can be regulated by microRNAs (miR-195-5p) due to the number of stable hydrogen atoms observed within the distance of 2.0 Å and the favorable amino acids (Ala221, Ile353, Ile365, Ile756, Val797, Val70, Val154, Ile159, Val347, Tyr804, Phe811, Tyr815, and Phe156) identified in the binding pocket of the argonaute protein. Due to the possibility of CHEK1’s involvement in solid tumors, it may potentially be a target for therapeutic intervention in cancer. Further studies into the interaction between CHEK1 and other co-expressed genes may give further insight into other modes of regulation of this gene in cancer patients.

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Section: Discussionmentioning

confidence: 99%

Gene Expression Alterations and Molecular Analysis of CHEK1 in Solid Tumors

Fadaka

Bakare

Sibuyi

et al. 2020

Cancers

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“…MicroRNA‐195 (miR‐195) is mapped to chromosome 17p13.1 and is one of the miR‐15/107 family members with a similar sequence (AGCAGC) . Accumulating evidence suggests that abnormal expression of miR‐195 may contribute to the pathogenesis of many diseases, including Alzheimer’s disease , heart failure and cerebral ischemia .…”

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confidence: 99%

Retracted: Demethylation of miR‐195 suppresses prostate cancer cell proliferation, migration and invasion

Zou

Chen

et al. 2020

FEBS Open Bio

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Prostate cancer (PCa) is the most prevalent cancer among men and the second leading cause of tumor‐associated deaths worldwide, with increasing incidence rates over the last 10 years. Recently, miR‐195 was reported to be hypermethylated at its promoter CpG island and down‐regulated in hepatocellular carcinoma. However, the function of miR‐195 and the underlying mechanisms in PCa remain unknown. Here, we report that a significant down‐regulation of microRNA‐195 (miR‐195) in PCa tissues and cell lines was associated with promoter methylation status. Overexpression of miR‐195 significantly suppressed cell proliferation, migration, invasion and epithelial–mesenchymal transition (increased E‐cadherin and decreased N‐cadherin) in PCa cells. We further demonstrated that transfection with a miR‐195 inhibitor reversed the inhibitory effect of the DNA methyltransferase inhibitor 5‐azacytidine on the proliferation, migration and invasion ability of PCa cells. In summary, our findings suggest that miR‐195 may function as a crucial tumor suppressor in PCa.

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“…Re-expression of the tumor-suppressor let-7 is another proposed miRNA therapeutic strategy to upregulate tumor-suppressor miRNA by exogenously transfecting with pre-let-7, which leads to the inhibition of growth [140]. In addition to tumor suppressor miRNAs, some of the miRNAs can serve as oncogenes and can be used as therapeutic targets for cancer, including miR-21, which is significantly overexpressed in many types of human cancers; thus, miR-21 is a potential therapeutic target for a certain cancer [146].…”

Section: Therapeutic Implications Of Mirna In Human Diseasesmentioning

confidence: 99%

Toxic-Metal-Induced Alteration in miRNA Expression Profile as a Proposed Mechanism for Disease Development

Wallace

Taalab

Heinze

et al. 2020

Cells

106

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Toxic metals are extensively found in the environment, households, and workplaces and contaminate food and drinking water. The crosstalk between environmental exposure to toxic metals and human diseases has been frequently described. The toxic mechanism of action was classically viewed as the ability to dysregulate the redox status, production of inflammatory mediators and alteration of mitochondrial function. Recently, growing evidence showed that heavy metals might exert their toxicity through microRNAs (miRNA)-short, single-stranded, noncoding molecules that function as positive/negative regulators of gene expression. Aberrant alteration of the endogenous miRNA has been directly implicated in various pathophysiological conditions and signaling pathways, consequently leading to different types of cancer and human diseases. Additionally, the gene-regulatory capacity of miRNAs is particularly valuable in the brain-a complex organ with neurons demonstrating a significant ability to adapt following environmental stimuli. Accordingly, dysregulated miRNAs identified in patients suffering from neurological diseases might serve as biomarkers for the earlier diagnosis and monitoring of disease progression. This review will greatly emphasize the effect of the toxic metals on human miRNA activities and how this contributes to progression of diseases such as cancer and neurodegenerative disorders (NDDs).

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MicroRNA-195: a review of its role in cancers

Cited by 68 publications

References 174 publications

Gene Expression Alterations and Molecular Analysis of CHEK1 in Solid Tumors

Gene Expression Alterations and Molecular Analysis of CHEK1 in Solid Tumors

Retracted: Demethylation of miR‐195 suppresses prostate cancer cell proliferation, migration and invasion

Toxic-Metal-Induced Alteration in miRNA Expression Profile as a Proposed Mechanism for Disease Development

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