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microRNA-103 Contributes to Progression of Polycystic Ovary Syndrome Through Modulating the IRS1/PI3K/AKT Signal Axis.
Arch Med Res. 2021 07; 52(5):494-504.AM

Abstract

BACKGROUND

Polycystic ovary syndrome (PCOS) is a frequent gynecological endocrine disorder, and the majority of PCOS patients experience different degrees of insulin resistance (IR). Nevertheless, the functions of microRNAs (miRNAs) in IR of PCOS remain unclear. In this study, we desired to elucidate the mechanisms of miR-103 in IR of PCOS.

METHODS

The ovarian pathological morphology of established PCOS rats was detected by HE staining. Following miR-103 expression determination in the ovarian tissues of PCOS rats, the relationship between its expression and IR was studied. A PCOS/IR cell model was established, and the effect of miR-103 on granulosa cells was determined by CCK-8 assay and flow cytometry. Through online website prediction and consulting related literatures, the target gene of miR-103 and the pathway regulated by the target genes were discovered, which was verified by further experiments.

RESULTS

PCOS rats showed polycystic changes in the ovary and a decrease in granulosa cells, and these symptoms were more pronounced in rats showed IR. miR-103 expressed highly in PCOS and was positively related to IR. miR-103 inhibitor led to improved PCOS-related symptoms. In addition, miR-103 directly targeted IRS1, which was poorly expressed in PCOS, and IRS1 silencing promoted PCOS development. Furthermore, miR-103 regulated the PI3K/AKT pathway by targeting IRS1, and PI3K/AKT pathway suppression reduced the therapeutic effect of miR-103 inhibitor.

CONCLUSION

This study indicates that miR-103 disrupts the PI3K/AKT pathway activation by targeting IRS1, thereby aggravating PCOS development. miR-103 inhibition may be a promising molecular target for treatment of PCOS.

Links

Publisher Full Text (DOI)

Authors+Show Affiliations

Mu J
Department of Endocrinology, the Second Affiliated Hospital of Harbin Medical University, Harbin 150001, Heilongjiang, P.R. China; Department of Endocrinology, Shenzhen SAMII Medical Center, Shenzhen 518118, Guangdong, P.R. China.
Yu P
Department of Endocrinology, Shenzhen SAMII Medical Center, Shenzhen 518118, Guangdong, P.R. China.
Li Q
Department of Endocrinology, the Second Affiliated Hospital of Harbin Medical University, Harbin 150001, Heilongjiang, P.R. China. Electronic address: qiangli01163@163.com.

MeSH

AnimalsFemaleGranulosa CellsInsulin Receptor Substrate ProteinsMicroRNAsPhosphatidylinositol 3-KinasesPolycystic Ovary SyndromeProto-Oncogene Proteins c-aktRatsSignal Transduction

Pub Type(s)

Journal Article

Language

eng

PubMed ID

33583602

Citation

Mu, Jiawei, et al. "MicroRNA-103 Contributes to Progression of Polycystic Ovary Syndrome Through Modulating the IRS1/PI3K/AKT Signal Axis." Archives of Medical Research, vol. 52, no. 5, 2021, pp. 494-504.
Mu J, Yu P, Li Q. MicroRNA-103 Contributes to Progression of Polycystic Ovary Syndrome Through Modulating the IRS1/PI3K/AKT Signal Axis. Arch Med Res. 2021;52(5):494-504.
Mu, J., Yu, P., & Li, Q. (2021). MicroRNA-103 Contributes to Progression of Polycystic Ovary Syndrome Through Modulating the IRS1/PI3K/AKT Signal Axis. Archives of Medical Research, 52(5), 494-504. https://doi.org/10.1016/j.arcmed.2021.01.008
Mu J, Yu P, Li Q. MicroRNA-103 Contributes to Progression of Polycystic Ovary Syndrome Through Modulating the IRS1/PI3K/AKT Signal Axis. Arch Med Res. 2021;52(5):494-504. PubMed PMID: 33583602.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - microRNA-103 Contributes to Progression of Polycystic Ovary Syndrome Through Modulating the IRS1/PI3K/AKT Signal Axis. AU - Mu,Jiawei, AU - Yu,Ping, AU - Li,Qiang, Y1 - 2021/02/11/ PY - 2020/05/28/received PY - 2020/10/31/revised PY - 2021/01/21/accepted PY - 2021/2/16/pubmed PY - 2021/12/15/medline PY - 2021/2/15/entrez KW - IRS1 KW - Insulin resistance KW - PI3K/AKT pathway KW - Polycystic ovary syndrome KW - microRNA-103 SP - 494 EP - 504 JF - Archives of medical research JO - Arch Med Res VL - 52 IS - 5 N2 - BACKGROUND: Polycystic ovary syndrome (PCOS) is a frequent gynecological endocrine disorder, and the majority of PCOS patients experience different degrees of insulin resistance (IR). Nevertheless, the functions of microRNAs (miRNAs) in IR of PCOS remain unclear. In this study, we desired to elucidate the mechanisms of miR-103 in IR of PCOS. METHODS: The ovarian pathological morphology of established PCOS rats was detected by HE staining. Following miR-103 expression determination in the ovarian tissues of PCOS rats, the relationship between its expression and IR was studied. A PCOS/IR cell model was established, and the effect of miR-103 on granulosa cells was determined by CCK-8 assay and flow cytometry. Through online website prediction and consulting related literatures, the target gene of miR-103 and the pathway regulated by the target genes were discovered, which was verified by further experiments. RESULTS: PCOS rats showed polycystic changes in the ovary and a decrease in granulosa cells, and these symptoms were more pronounced in rats showed IR. miR-103 expressed highly in PCOS and was positively related to IR. miR-103 inhibitor led to improved PCOS-related symptoms. In addition, miR-103 directly targeted IRS1, which was poorly expressed in PCOS, and IRS1 silencing promoted PCOS development. Furthermore, miR-103 regulated the PI3K/AKT pathway by targeting IRS1, and PI3K/AKT pathway suppression reduced the therapeutic effect of miR-103 inhibitor. CONCLUSION: This study indicates that miR-103 disrupts the PI3K/AKT pathway activation by targeting IRS1, thereby aggravating PCOS development. miR-103 inhibition may be a promising molecular target for treatment of PCOS. SN - 1873-5487 UR - https://www.unboundmedicine.com/medline/citation/33583602/microRNA_103_Contributes_to_Progression_of_Polycystic_Ovary_Syndrome_Through_Modulating_the_IRS1/PI3K/AKT_Signal_Axis_ DB - PRIME DP - Unbound Medicine ER -
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