Research Progress on Post-Translational Modification in Polycystic Ovary Syndrome

doi:10.12280/gjszjk.20230372

Abstract

Abstract:

Polycystic ovary syndrome (PCOS) is one of the most common endocrine disorders in women, but its pathogenesis is unknown. Current researches suggested that the disease may be influenced by a variety of factors, including epigenetic and environmental factors. In recent years, the incidence of PCOS has been increasing, leading to a decline in the quality of life of patients. Therefore, it is necessary to actively explore new treatments. Post-translational modification (PTM) is an important way to regulate protein function. Most studies have found that phosphorylation is closely related to insulin resistance of PCOS, acetylation is mainly focused on the quality of PCOS oocytes, and methylation is closely related to PCOS lipid metabolism. Exploring the role of PTM in the occurrence and development of PCOS may provide new ideas for targeted treatment of this disease.

Key words: Polycystic ovary syndrome, Protein processing, post-translational, Phosphorylation, Acetylation, Methylation, Ubiquitination

LIU Yi-ran, FENG Rui-zhi, QIAN Yun. Research Progress on Post-Translational Modification in Polycystic Ovary Syndrome[J]. Journal of International Reproductive Health/Family Planning, 2024, 43(1): 38-42.

References 29

[1]	Sanchez-Garrido MA, Tena-Sempere M. Metabolic dysfunction in polycystic ovary syndrome: Pathogenic role of androgen excess and potential therapeutic strategies[J]. Mol Metab, 2020, 35:100937. doi: 10.1016/j.molmet.2020.01.001.
[2]	Tran TQ, Lowman XH, Kong M. Molecular Pathways: Metabolic Control of Histone Methylation and Gene Expression in Cancer[J]. Clin Cancer Res, 2017, 23(15):4004-4009. doi: 10.1158/1078-0432.CCR-16-2506. pmid: 28404599
[3]	Zhong Q, Xiao X, Qiu Y, et al. Protein posttranslational modifications in health and diseases: Functions, regulatory mechanisms, and therapeutic implications[J]. MedComm(2020), 2023, 4(3):e261. doi: 10.1002/mco2.261.
[4]	Pan L, Feng F, Wu J, et al. Demethylzeylasteral targets lactate by inhibiting histone lactylation to suppress the tumorigenicity of liver cancer stem cells[J]. Pharmacol Res, 2022, 181:106270. doi: 10.1016/j.phrs.2022.106270.
[5]	Yang Z, Yan C, Ma J, et al. Lactylome analysis suggests lactylation-dependent mechanisms of metabolic adaptation in hepatocellular carcinoma[J]. Nat Metab, 2023, 5(1):61-79. doi: 10.1038/s42255-022-00710-w. pmid: 36593272
[6]	Deng L, Chen L, Zhao L, et al. Ubiquitination of Rheb governs growth factor-induced mTORC1 activation[J]. Cell Res, 2019, 29(2):136-150. doi: 10.1038/s41422-018-0120-9. pmid: 30514904
[7]	Xu G, Wu Y, Xiao T, et al. Multiomics approach reveals the ubiquitination-specific processes hijacked by SARS-CoV-2[J]. Signal Transduct Target Ther, 2022, 7(1):312. doi: 10.1038/s41392-022-01156-y.
[8]	Kebede AF, Nieborak A, Shahidian LZ, et al. Histone propionylation is a mark of active chromatin[J]. Nat Struct Mol Biol, 2017, 24(12):1048-1056. doi: 10.1038/nsmb.3490. pmid: 29058708
[9]	Zeng J, Aryal RP, Stavenhagen K, et al. Cosmc deficiency causes spontaneous autoimmunity by breaking B cell tolerance[J]. Sci Adv, 2021, 7(41):eabg9118. doi: 10.1126/sciadv.abg9118.
[10]	Zhu Q, Wang H, Chai S, et al. O-GlcNAcylation promotes tumor immune evasion by inhibiting PD-L1 lysosomal degradation[J]. Proc Natl Acad Sci U S A, 2023, 120(13):e2216796120. doi: 10.1073/pnas.2216796120.
[11]	Min Z, Long X, Zhao H, et al. Protein Lysine Acetylation in Ovarian Granulosa Cells Affects Metabolic Homeostasis and Clinical Presentations of Women With Polycystic Ovary Syndrome[J]. Front Cell Dev Biol, 2020, 8:567028. doi: 10.3389/fcell.2020.567028.
[12]	Mao Z, Li T, Zhao H, et al. Methylome and transcriptome profiling revealed epigenetic silencing of LPCAT1 and PCYT1A associated with lipidome alterations in polycystic ovary syndrome[J]. J Cell Physiol, 2021, 236(9):6362-6375. doi: 10.1002/jcp.30309.
[13]	Liu M, Zhu H, Zhu Y, et al. Guizhi Fuling Wan reduces autophagy of granulosa cell in rats with polycystic ovary syndrome via restoring the PI3K/AKT/mTOR signaling pathway[J]. J Ethnopharmacol, 2021, 270:113821. doi: 10.1016/j.jep.2021.113821.
[14]	Qiu Z, Dong J, Xue C, et al. Liuwei Dihuang Pills alleviate the polycystic ovary syndrome with improved insulin sensitivity through PI3K/Akt signaling pathway[J]. J Ethnopharmacol, 2020, 250:111965. doi: 10.1016/j.jep.2019.111965.
[15]	Wu C, Jiang F, Wei K, et al. Exercise activates the PI3K-AKT signal pathway by decreasing the expression of 5α-reductase type 1 in PCOS rats[J]. Sci Rep, 2018, 8(1):7982. doi: 10.1038/s41598-018-26210-0. pmid: 29789599
[16]	陈东思. IRS-1及ERK2丝氨酸磷酸化与PCOS患者IR的关系[D]. 青岛: 青岛大学, 2016.
[17]	Wang Y, Zeng Z, Zhao S, et al. Humanin Alleviates Insulin Resistance in Polycystic Ovary Syndrome: A Human and Rat Model-Based Study[J]. Endocrinology, 2021, 162(8):bqab056. doi: 10.1210/endocr/bqab056.
[18]	Shen H, Xu X, Fu Z, et al. The interactions of CAP and LYN with the insulin signaling transducer CBL play an important role in polycystic ovary syndrome[J]. Metabolism, 2022, 131:155164. doi: 10.1016/j.metabol.2022.155164.
[19]	Wei Y, Wang Z, Wei L, et al. MicroRNA-874-3p promotes testosterone-induced granulosa cell apoptosis by suppressing HDAC1-mediated p53 deacetylation[J]. Exp Ther Med, 2021, 21(4):359. doi: 10.3892/etm.2021.9790. pmid: 33732332
[20]	Eini F, Novin MG, Joharchi K, et al. Intracytoplasmic oxidative stress reverses epigenetic modifications in polycystic ovary syndrome[J]. Reprod Fertil Dev, 2017, 29(12):2313-2323. doi: 10.1071/RD16428.
[21]	Hosseini E, Shahhoseini M, Afsharian P, et al. Role of epigenetic modifications in the aberrant CYP19A1 gene expression in polycystic ovary syndrome[J]. Arch Med Sci, 2019, 15(4):887-895. doi: 10.5114/aoms.2019.86060. pmid: 31360184
[22]	Roy S, Abudu A, Salinas I, et al. Androgen-mediated Perturbation of the Hepatic Circadian System Through Epigenetic Modulation Promotes NAFLD in PCOS Mice[J]. Endocrinology, 2022, 163(10):bqac127. doi: 10.1210/endocr/bqac127.
[23]	Rudnicka E, Suchta K, Grymowicz M, et al. Chronic Low Grade Inflammation in Pathogenesis of PCOS[J]. Int J Mol Sci, 2021, 22(7):3789. doi: 10.3390/ijms22073789.
[24]	Guo X, Puttabyatappa M, Thompson RC, et al. Developmental Programming: Contribution of Epigenetic Enzymes to Antral Follicular Defects in the Sheep Model of PCOS[J]. Endocrinology, 2019, 160(10):2471-2484. doi: 10.1210/en.2019-00389. pmid: 31398247
[25]	康亚妮, 毛湛睿, 王昱欢, 等. DNA甲基化标志物PCYT1A在制备诊断PCOS试剂盒中的应用[P]. 上海市:CN202010124607.6. 2020-06-09.
[26]	Filippou P, Homburg R. Is foetal hyperexposure to androgens a cause of PCOS?[J]. Hum Reprod Update, 2017, 23(4):421-432. doi: 10.1093/humupd/dmx013. pmid: 28531286
[27]	Mimouni N, Paiva I, Barbotin AL, et al. Polycystic ovary syndrome is transmitted via a transgenerational epigenetic process[J]. Cell Metab, 2021, 33(3):513-530.e8. doi: 10.1016/j.cmet.2021.01.004. pmid: 33539777
[28]	Li Y, Xiang Y, Song Y, et al. MALAT1 downregulation is associated with polycystic ovary syndrome via binding with MDM2 and repressing P53 degradation[J]. Mol Cell Endocrinol, 2022, 543:111528. doi: 10.1016/j.mce.2021.111528.
[29]	Liu X, Sun C, Zou K, et al. Novel PGK1 determines SKP2-dependent AR stability and reprograms granular cell glucose metabolism facilitating ovulation dysfunction[J]. EBioMedicine, 2020, 61:103058. doi: 10.1016/j.ebiom.2020.103058.