miR-142-5p enhances cisplatin-induced apoptosis in ovarian cancer cells by targeting multiple anti-apoptotic genes

Li, Xiaodi; Chen, Wei; Jin, Yuhao; Xue, Renxing; Su, Jiancheng; Mu, Zekun; Li, Jiamin; Jiang, Siqi

doi:10.1016/j.bcp.2019.01.009

Cited by 86 publications

(50 citation statements)

References 67 publications

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“…Inspired by former findings that miR‐142‐5p is down‐regulated in IL‐1β‐stimulated chondrocytes, we further validated the function of miR‐142‐5p on chondrocyte growth and ECM synthesis in the present study. Previously, miR‐142‐5p was found to be tumor‐suppressing in lung adenocarcinoma, pancreatic cancer and gastric cancer, and was reported to be cisplatin‐related in ovarian cancer . Additionally, miR‐142‐5p is associated with peripheral immune tolerance, as well as a profibrogenic macrophage program .…”

Section: Discussionmentioning

confidence: 99%

miR‐142‐5p protects against osteoarthritis through competing with lncRNA XIST

Sun

et al. 2020

The Journal of Gene Medicine

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Background The relevance between abnormal microRNA expression and osteoarthritis (OA) has been elaborated in recent studies. Hence, the present study aimed to assess the impact of miR‐142‐5p on chondrocyte growth and apoptosis. Methods To mimic OA‐like chondrocyte damage, interleukin (IL)‐1β was used for chondrocyte treatment. The expression of miR‐142‐5p, SGTB, long non‐coding RNA (lncRNA) X inactive specific transcript (XIST) and involved molecules such as Col2A1, Bcl‐2, MMP13 and Bax was determined via a quantitative reverse transcriptase‐polymerase chain reaction and western blot analyses. Functional roles of miR‐142‐5p, SGTB and XIST were monitored in 5‐ethynyl‐2'‐deoxyuridine, CCK‐8 and TUNEL experiments. Rescue analyses were conducted to consolidate the effect of the XIST/miR‐142‐5p/SGTB axis on chondrocytes in OA. Results miR‐142‐5p was down‐regulated in IL‐1β‐treated chondrocytes, whereas SGTB and XIST levels were increased. Overexpression of miR‐142‐5p stimulated proliferation and retarded apoptosis in IL‐1β‐treated chondrocytes. Meanwhile, miR‐142‐5p elevation was correlated with an elevation of Col2A1 and Bcl‐2, as well as a decline of MMP13 and Bax. A mechanistic study showed that miR‐142‐5p negatively regulated SGTB expression. Moreover, we found that lncRNA XIST could relieve the inhibition of miR‐142‐5p on SGTB expression. Augmentation of SGTB or suppression of miR‐142‐5p reversed the influence of XIST depletion on chondrocyte growth and apoptosis. Conclusions The present study has explored the fundamental role of miR‐142‐5p in IL‐1β‐treated chondrocytes, as well as the novel molecular mechanism constituted by miR‐142‐5p/SGTB/XIST in OA. Potentially, the results obtained may add new insight into OA pathogenesis.

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Section: Discussionmentioning

confidence: 99%

miR‐142‐5p protects against osteoarthritis through competing with lncRNA XIST

Sun

et al. 2020

The Journal of Gene Medicine

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“…The proto-oncogenic role of MCL1 gene in OVC has been identified by various studies during the last decade. 14,[21][22][23] These studies not only reported the important antiapoptotic effects of MCL1 gene on OVC but also showed that this gene had a critical function in drug resistance of OVC. MCL1 protein interacts with a wide spectra of other proteins to interfere with normal cell apoptosis such as deubiquitinating enzyme 3, ubiquitin-specific proteases, and BH3-only protein NOXA etc.…”

Section: Discussionmentioning

confidence: 99%

“…The proto‐oncogenic role of MCL1 gene in OVC has been identified by various studies during the last decade . These studies not only reported the important antiapoptotic effects of MCL1 gene on OVC but also showed that this gene had a critical function in drug resistance of OVC.…”

Section: Discussionmentioning

confidence: 99%

“…Then in 2013, Rao et al found that miR‐106a inhibited OVC cell A2780's survival by suppressing MCL1 gene expression. Then there were miR‐29b, miR‐491‐5p, miR‐509‐3p,, and miR‐142‐5p that were subsequently reported to play proto‐oncogenic or anti‐oncogenic roles in OVC initiation and progression . The target miRNAs varies; however, the working mechanisms are similar.…”

Section: Discussionmentioning

confidence: 99%

“…Then there were miR-29b, miR-491-5p, miR-509-3p,, and miR-142-5p that were subsequently reported to play proto-oncogenic or anti-oncogenic roles in OVC initiation and progression. 10,22,29,30 The target miRNAs varies; however, the working mechanisms are similar. We reckon that a complicated network exists while cancer The difference among the groups was analyzed using one-way ANOVA.…”

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

miR‐153‐3p regulates progression of ovarian carcinoma in vitro and in vivo by targeting MCL1 gene

Cui

Zhang

Zhao

et al. 2019

J of Cellular Biochemistry

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The study of either miR‐153‐3p or MCL1 gene in ovarian carcinoma (OVC) has been reported; however, the interaction between miR‐153‐3p and MCL1 gene in OVC as well as the influence of their interaction on OVC progression has not been reported yet. Herein we intended to study the effects of miR‐153‐3p/MCL1 axis in OVC. Web‐based bioinformatics algorithms including DIANA TarBase 8.0, PicTar, and TargetScan Human 7.2 were used to predict the microRNAs (miRNAs) that could target MCL1 mRNA. Patient characteristics data collection and tissue sample immunohistochemical staining were used to determine the expression level of miR‐153‐3p and MCL1. We determined to unravel the effects of the pairing‐up of miR‐153‐3p and MCL1 mRNA in OVC cell lines (OVCAR3 cell line and A2780) and xenografts (immunodeficient(immunodeficient Rag−/− mice) using several methods including real‐time quantitative reverse transcription polymerase chain reaction, westernWestern blot, colony formation assay, wound healing assay, Transwell invasion assay, flow cytometry assay, and xenograft assay. These experiments were performed to study OVC cellular activities such as cell growth and death and so forth in vitro and in vivo. Plenty of miRNAs that can target MCL1 mRNA have been identified, and we have narrowed them down to miR‐153‐3p. MCL1 gene was found overexpressed in OVC tissues and OVC cell lines at RNA and protein levels, whereas miR‐153‐3p was found under‐expressed in OVC tissues and cells. miR‐153‐3p was found to target MCL1 mRNA and interfered OVC progression. The repression of MCL1 gene expression caused by either miR‐153‐3p or small interfering RNA technique led to significantly reduced OVC cell growth and invasion in vitro. Lastly, the engraftment of transfected human OVC cells into Rag−/− mice confirmed the in vitro results. MCL1 gene acts as a cancer facilitator in OVC. In this study, we revealed the role of miR‐153‐3p on OVC progression by targeting MCL1 gene. Our work could comprehend the current understanding of OVC progression and contribute to the underlying aggression mechanism of this cancer.

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Identification of lncRNA–miRNA–mRNA regulatory network associated with epithelial ovarian cancer cisplatin‐resistant

Zhao

Tang

Zuo

et al. 2019

Journal Cellular Physiology

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To construct a long noncoding RNA (lncRNA)-microRNA (miRNA)-messenger RNA (mRNA) regulatory network related to epithelial ovarian cancer (EOC) cisplatinresistant, differentially expressed genes (DEGs), differentially expressed lncRNAs (DELs), and differentially expressed miRNAs (DEMs) between MDAH and TOV-112D cells lines were identified. Gene Ontology (GO) analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were conducted to analyze the biological functions of DEGs. Downstream mRNAs or upstream lncRNAs for miRNAs were analyzed at miRTarBase 7.0 or DIANA-LncBase V2, respectively. A total of 485 significant DEGs, 85 DELs, and 5 DEMs were identified. Protein-protein interaction (PPI) network of DEGs contrains 81 nodes and 141 edges was constructed, and 25 hub genes related to EOC cisplatin-resistant were identified. Subsequently, a lncRNA-miRNA-mRNA regulatory network contains 4 lncRNAs, 4 miRNAs, and 35 mRNAs was established. Taken together, our study provided evidence concerning the alteration genes involved in EOC cisplatin-resistant, which will help to unravel the mechanisms underlying drug resistant. K E Y W O R D S cisplatin-resistant, epithelial ovarian cancer, lncRNA, miRNA, mRNA

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miR-142-5p enhances cisplatin-induced apoptosis in ovarian cancer cells by targeting multiple anti-apoptotic genes

Cited by 86 publications

References 67 publications

miR‐142‐5p protects against osteoarthritis through competing with lncRNA XIST

miR‐142‐5p protects against osteoarthritis through competing with lncRNA XIST

miR‐153‐3p regulates progression of ovarian carcinoma in vitro and in vivo by targeting MCL1 gene

Identification of lncRNA–miRNA–mRNA regulatory network associated with epithelial ovarian cancer cisplatin‐resistant

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