MicroRNA-93 Promotes Epithelial–Mesenchymal Transition of Endometrial Carcinoma Cells

Chen, Shuo; Chen, Xi; Sun, Kaixuan; Xiu, Yin-Ling; Liu, Bo-Liang; Feng, Min; Sang, Xiu-Bo; Zhao, Yang

doi:10.1371/journal.pone.0165776

Cited by 30 publications

(37 citation statements)

References 39 publications

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“…Increasing evidence has indicated that miRNAs exert biological functions in cancer cells by suppressing the expression of target genes (31,33). Bioinformatics analysis using TargetScan indicated that PTEN may be a potential target of miR-93-5p as determined in the present study.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑93‑5p promotes the progression of human retinoblastoma by regulating the PTEN/PI3K/AKT signaling pathway

et al. 2018

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Numerous repor ts have indicated that microRNA-93-5p (miR-93-5p) is involved in the development and progression of human cancer, including non-small cell lung, gastric and breast cancer; however, the role of miR-93-5p in retinoblastoma (RB) remains unknown. In the present study, it was reported that miR-93-5p expression levels were significantly upregulated in RB tissues compared with in normal tissues by reverse transcription-quantitative polymerase chain reaction. Furthermore, it was demonstrated via cell counting kit-8 and Transwell assays that knockdown of miR-93-5p significantly suppressed the proliferation, migration and invasion of RB cells, but promoted cellular apoptosis. Regarding the underlying mechanism, the present study reported that phosphatase and tensin homolog (PTEN) was a direct target of miR-93-5p in RB cells. Overexpression of miR-93-5p significantly inhibited the expression of PTEN; opposing results were observed when PTEN expression was downregulated. Furthermore, the present study revealed that PTEN expression levels were downregulated and were inversely correlated with that of miR-93-5p in RB tissues. Additionally, the present study demonstrated that knockdown of PTEN in miR-93-5p-depleted RB cells significantly reversed the effects of miR-93-5p on cell proliferation, migration and invasion; miR-93-5p knockdown was suggested to promote PTEN expression, consequently inhibiting the activation of phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway. Collectively, the results of the present study demonstrated that miR-93-5p may serve a role as an oncogene by modulating the PTEN/PI3K/AKT signaling pathway in RB, indicating that miR-93-5p may be a potential therapeutic target for the treatment of RB.

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Section: Discussionmentioning

confidence: 99%

MicroRNA‑93‑5p promotes the progression of human retinoblastoma by regulating the PTEN/PI3K/AKT signaling pathway

et al. 2018

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“…In 2014, Liu et al (22) reported that 12 miRNAs were abnormally expressed in SUI, including two groups: In the upregulated group were let-7a, miR-101, miR-125b-2, miR-190b and miR-892b; in the downregulated group were miR-124, miR-330-3p, miR-485-3p, miR-517b, miR-523, miR-589, and miR-93. IN addition, miR-93 has been reported to be involved in a number of diseases and to be abnormally expressed in the progression and tumorigenesis of a number of types of cancer, including endometrial, lung, breast, hepatocellular, pancreatic, colorectal and ovarian cancer (23). However, the roles of miRNA in SUI remain unclear.…”

Section: Discussionmentioning

confidence: 99%

“…The results demonstrated that miR-93 was able to bind to CAPN2; additionally, overexpression of miR-93 decreased the expression of calpain-2, which suggested that calpain-2 may be a direct target of miR-93. As the primary components of the urethral support tissues are connective tissues which contain a large number of ECM components, and ECM metabolism is regulated by degradative enzyme matrix metalloproteinases (MMPs) (23,24), degradative enzyme inhibitors and tissue inhibitors of metalloproteinases may be altered in patients with SUI. In the present study, it was observed that MMP1 was upregulated in the vaginal wall tissues of patients with SUI and in SUI primary fibroblasts, suggesting that MMP1 may be negatively regulated by miR-93, which was consistent with a previous report (14).…”

Section: Discussionmentioning

confidence: 99%

miR-93‑mediated collagen expression in stress urinary incontinence via calpain-2

Yang

Wang

et al. 2017

Mol Med Report

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The aim of the present study was to investigate the expression and mechanism of microRNA (miR)‑93 in collagen expression in stress urinary incontinence (SUI). Vaginal tissue, primary fibroblasts and SUI primary fibroblasts were obtained to detect the expression of miR‑93, interstitial collagenase (MMP1), collagen I and calpain‑2. Reverse transcription‑quantitative polymerase chain reaction analysis was performed to detect the levels of miR‑93 and MMP1. Western blotting was used to evaluate the protein levels of calpain‑2, MMP1 and collagen I. MMP1 and hydroxyproline levels in the supernatant were measured by ELISA. The association between miR‑93 and calpain‑2 was investigated by luciferase reporter assays. The expression of miR‑93 and collagen I was significantly downregulated in the SUI group, while the expression of calpain‑2 and MMP1 was significantly upregulated. ELISA analysis demonstrated that the MMP1 level increased and the hydroxyproline level decreased in the SUI group. Additionally, calpain‑2 was identified to be a target of miR‑93, and miR‑93 was able to negatively regulate the expression of calpain‑2. Restoration of calpain‑2 in miR‑93‑overexpresseing SUI primary fibroblasts reversed the alteration in hydroxyproline expression, indicating that calpain‑2 was negatively associated with collagen expression. The results of the present study suggested that miR‑93 regulated MMP1 and collagen I expression in fibroblasts via calpain‑2. miR‑93 mediated collagen expression in stress urinary incontinence via calpain‑2.

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“…Therefore, the random effect model was selected. The overall sensitivity, specificity, positive likelihood ratio (PLR), negative likelihood ratio (NLR), diagnostic odds ratio (DOR), and AUC were 0.76 (0.64-0.85), 0.82 (0.64-0.92), 4.2 (2.2-8.1), 0.29 (0.22-0.40), 14 (8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25), and 0.85 (0.82-0.88), respectively, suggesting the excellent potential diagnostic capability of miR-93 in various human cancers. Subgroup analyses based on ethnicity, sample type, and expression level were performed ( Table 2).…”

Section: The Diagnostic Meta-analysismentioning

confidence: 99%

Molecular mechanism and role of microRNA‐93 in human cancers: A study based on bioinformatics analysis, meta‐analysis, and quantitative polymerase chain reaction validation

Gao

Deng

Liu

et al. 2018

J of Cellular Biochemistry

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Introduction Currently, studies have shown that microRNA‐93 (miR‐93) can be an oncogene or a tumor suppressor in different kinds of cancers. The role of miR‐93 in human cancers is inconsistent and the underlying mechanism on the aberrant expression of miR‐93 is complicated. Methods We first conducted gene enrichment analysis to give insight into the prospective mechanism of miR‐93. Second, we performed a meta‐analysis to evaluate the clinical value of miR‐93. Finally, a validation test based on quantitative polymerase chain reaction (qPCR) was performed to further investigate the role of miR‐93 in pan‐cancer. Results Gene Ontology (GO) enrichment analysis results showed that the target genes of miR‐93 were closely related to transcription, and MAPK1, RBBP7 and Smad7 became the hub genes. In the diagnostic meta‐analysis, the overall sensitivity, specificity, and area under the curve were 0.76 (0.64‐0.85), 0.82 (0.64‐0.92), and 0.85 (0.82‐0.88), respectively, which suggested that miR‐93 had excellent performance on the diagnosis for human cancers. In the prognostic meta‐analysis, dysregulated miR‐93 was found to be associated with poor OS in cancer patients. In the qPCR validation test, the serum levels of miR‐93 were upregulated in breast cancer, breast hyperplasia, lung cancer, chronic obstructive pulmonary disease, nasopharyngeal cancer, hepatocellular cancer, gastric ulcer, endometrial cancer, esophageal cancer, laryngeal cancer, and prostate cancer compared with healthy controls. Conclusions miR‐93 could act as an effective diagnostic and prognostic factor for cancer patients. Its clinical value for cancer early diagnosis and survival prediction is promising.

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MicroRNA-93 Promotes Epithelial–Mesenchymal Transition of Endometrial Carcinoma Cells

Cited by 30 publications

References 39 publications

MicroRNA‑93‑5p promotes the progression of human retinoblastoma by regulating the PTEN/PI3K/AKT signaling pathway

MicroRNA‑93‑5p promotes the progression of human retinoblastoma by regulating the PTEN/PI3K/AKT signaling pathway

miR-93‑mediated collagen expression in stress urinary incontinence via calpain-2

Molecular mechanism and role of microRNA‐93 in human cancers: A study based on bioinformatics analysis, meta‐analysis, and quantitative polymerase chain reaction validation

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