Pashaei Maryam, Mashayekhi Farhad, Zahiri Ziba, Salehi Zivar
Department of Biology, Faculty of Sciences, University of Guilan, Rasht, Iran.
Reproductive Health Research Centre, Department of Obstetrics & Gynaecology, Alzahra Hospital, School of Medicine, Guilan University of Medical Sciences, Rasht, Iran.
Gynecol Endocrinol. 2022 Jul;38(7):603-607. doi: 10.1080/09513590.2022.2076830. Epub 2022 May 19.
Many genes and miRNAs have been shown to be associated with the pathogenesis of endometriosis. (p63) is implicated in lineage specification, proliferative potential, differentiation, cell death and survival. The proto-oncogene encodes a cytoplasmic and nuclear protein tyrosine kinase implicated in cell differentiation, cell division, and cell adhesion. Moreover, hsa-miR-203a-3p was reported to play pivotal roles in tumor progression by targeting multiple genes, including and . The aim of this study was to investigate the expression of , , and miR-203a-3p in endometriosis.
This study included 30 women with endometriosis (stage III: = 12 and stage IV: = 18) and 30 age-matched controls. Total RNA extraction and cDNA synthesis were performed, and a quantitative polymerase chain reaction technique was used to determine the expression of miR-203a-3p, , and .
and were significantly overexpressed in stages III and IV endometriosis as compared to controls ( < .0001). Moreover, overexpression of and was observed in stage IV compared to stage III ( = .0006 and = .0002, respectively). Furthermore, significant increase miR-203a-3p expression has been seen in stage IV endometriosis compared to controls ( = .006). The expression of miR-203a-3p in stage III was not significant compared to stage IV and control ( = .33 and = .43, respectively).
It is concluded that miR-203a-3p, and gene expression is altered in the endometrium of patients with endometriosis. It is also suggested that miR-203a-3p, , and might be candidate factors for the pathogenesis of endometriosis and suggesting its therapeutic potential in endometriosis.
许多基因和微小RNA（miRNA）已被证明与子宫内膜异位症的发病机制有关。p63参与谱系特化、增殖潜能、分化、细胞死亡和存活。原癌基因编码一种细胞质和核蛋白酪氨酸激酶，参与细胞分化、细胞分裂和细胞黏附。此外，据报道，hsa-miR-203a-3p通过靶向多个基因（包括[具体基因未给出]和[具体基因未给出]）在肿瘤进展中发挥关键作用。本研究的目的是调查p63、[具体基因未给出]和miR-203a-3p在子宫内膜异位症中的表达情况。
本研究纳入30例子宫内膜异位症患者（III期：n = 12；IV期：n = 18）和30例年龄匹配的对照。进行总RNA提取和cDNA合成，并采用定量聚合酶链反应技术测定miR-203a-3p、p63和[具体基因未给出]的表达。
与对照组相比，III期和IV期子宫内膜异位症中p63和[具体基因未给出]显著过表达（P <.0001）。此外，与III期相比，IV期观察到p63和[具体基因未给出]过表达（分别为P = 0.0006和P = 0.0002）。此外，与对照组相比，IV期子宫内膜异位症中miR-203a-3p表达显著增加（P = 0.006）。III期miR-203a-3p的表达与IV期和对照组相比无显著差异（分别为P = 0.33和P = 0.43）。
得出结论，子宫内膜异位症患者子宫内膜中miR-203a-3p、p63和[具体基因未给出]基因表达发生改变。还表明miR-203a-3p、p63和[具体基因未给出]可能是子宫内膜异位症发病机制的候选因素，并提示其在子宫内膜异位症中的治疗潜力。
