Literature DB >> 31938287

miR-24-3p stimulates migration, invasion and proliferation of prostate cancer cells by targeting suppressor of cytokine signaling 6.

Yang Lin1, Huifang Cao2, Yuxin Tian1, Xinping Yang1, Changdong Zhou1, Qifu Zhang1.   

Abstract

Prostate cancer is among the most widespread malignancies affecting men in the world. Its aggressive evolution has been associated with altered expression of suppressor of cytokine signaling 6 (SOCS6) but very little is known about the mechanism by which this alteration occurs. The purpose of this study was to explore the role of SOCS6 in prostate cancer cells and the involvement of its regulating microRNA (miR), miR-24-3p. Prostate cancer cell lines were used to determine the transcription level of miR-24-3p and SOCS6 by quantitative reverse-transcriptase-polymerase chain reaction (qRT-PCR) and Western blot. Cell proliferation and cell migration assays were doneto determine the effect of miR-24-3p mimics and inhibitors on cell proliferation, invasion and migration. Luciferase reporter assay with SOCS6 3'-UTR was performed to confirm the control of SOCS6 expression by the miR. The results showed that miR-24-3p was up-regulated in prostate cancer cells whereas SOCS6 protein was downregulated. Overexpression of miR-24-3p in prostate cancer cells promoted cell proliferation, inhibited apoptosis, and increased cell migration and invasion. Luciferase reporter assays showed that SOCS6 is a direct target of its negative regulator miR-24-3p and overexpression of SOCS6 reverses the effects of miR-24-3p on the metastatic phenotype of prostate cancer cells. These results show case miR-24-3p up-regulation in prostate cancer and a mechanism for inhibition of SOCS6 expression. Thus, the miR-24-3p/SOCS6 pathway could be a relevant avenue for prostate cancer treatment. IJCEP
Copyright © 2018.

Entities:  

Keywords:  Prostate cancer; SOCS6; miR-24-3p

Year:  2018        PMID: 31938287      PMCID: PMC6958104     

Source DB:  PubMed          Journal:  Int J Clin Exp Pathol        ISSN: 1936-2625


  35 in total

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Journal:  Cell Death Differ       Date:  2017-05-12       Impact factor: 15.828

Review 2.  Suppression of cytokine signaling: the SOCS perspective.

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3.  Elevated expression of miR-24-3p is a potentially adverse prognostic factor in colorectal adenocarcinoma.

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Journal:  Clin Biochem       Date:  2016-12-07       Impact factor: 3.281

4.  MicroRNAs modulate the expression of the SOX18 transcript in lung squamous cell carcinoma.

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Review 6.  Cytokine expression and cancer detection.

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7.  miR-24-3p Suppresses Malignant Behavior of Lacrimal Adenoid Cystic Carcinoma by Targeting PRKCH to Regulate p53/p21 Pathway.

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Journal:  PLoS One       Date:  2016-04-13       Impact factor: 3.240

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2.  Urine Cell-Free MicroRNAs in Localized Prostate Cancer Patients.

Authors:  Yoko Koh; Matias A Bustos; Jamie Moon; Rebecca Gross; Romela Irene Ramos; Suyeon Ryu; Jane Choe; Selena Y Lin; Warren M Allen; David L Krasne; Timothy G Wilson; Dave S B Hoon
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Review 3.  Porcine Reproductive and Respiratory Syndrome Virus Evades Antiviral Innate Immunity via MicroRNAs Regulation.

Authors:  Xuan Zhang; Wen-Hai Feng
Journal:  Front Microbiol       Date:  2021-12-15       Impact factor: 5.640

4.  IL-1β promotes hypoxic vascular endothelial cell proliferation through the miR-24-3p/NKAP/NF-κB axis.

Authors:  Jiangnan Huang; Yumei Li; Zhiyuan Jiang; Lingjun Wu; Yueying Liu; Siwen Ma; Lang Li; Hui Wang
Journal:  Biosci Rep       Date:  2022-01-28       Impact factor: 3.840

5.  Herpes simplex virus 1 evades cellular antiviral response by inducing microRNA-24, which attenuates STING synthesis.

Authors:  Nikhil Sharma; Chenyao Wang; Patricia Kessler; Ganes C Sen
Journal:  PLoS Pathog       Date:  2021-09-30       Impact factor: 7.464

Review 6.  MicroRNAs as Potential Tools for Predicting Cancer Patients' Susceptibility to SARS-CoV-2 Infection and Vaccination Response.

Authors:  Tânia R Dias; Francisca Dias; Ana Luísa Teixeira; Hugo Sousa; Júlio Oliveira; Rui Medeiros
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7.  MiR-24-3p attenuates IL-1β-induced chondrocyte injury associated with osteoarthritis by targeting BCL2L12.

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