INVESTIGATION THE EXPRESSION LEVELS OF MIR-181 AND HOXA11 GENE IN EUTOPIC AND ECTOPIC ENDOMETRIAL TISSUE

被引:0
作者
Miraboutalebi, S. A. [1 ]
Ashkezari, M. Dehghani [1 ]
Seifati, S. M. [1 ]
机构
[1] Islamic Azad Univ, Med Biotechnol Res Ctr, Dept Biol, Ashkezar Branch, Yazd, Iran
关键词
miR-181; gene; HOXA11gene; endometriosis; ectopic tissue; utopic tissue; GYNECOLOGICAL CANCERS; IMPLANTATION WINDOW; WOMEN; MICRORNAS; BIOMARKERS; MECHANISMS; SPECTRUM;
D O I
10.4183/aeb.2024.33
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Objectives. The exact pathogenesis of the endometriosis is not apparent. MicroRNAs (miRNAs/miRs) are non-coding RNAs that regulate gene expression at the post- transcriptional level. MicroRNAs can be used a diagnostic and therapeutic tools in different disorders such as endometriosis. MiR-181 has a function in embryo implantation. The main aim of this study is to evaluate the expression of miR-181 and its relationship with HOXA11 gene expression in ectopic and eutopic endometrium tissues in women with endometriosis. Study design. Thirty-four women participated in this study. Ectopic tissue samples (N=17) were collected via laparoscopic surgery, and eutopic tissue samples (N=17) were obtained from an endometrial biopsy. Endometrial tissue samples without endometriosis were considered the control group. Tissue samples were placed in RNase-free microtube with RNAlaterTM Stabilization Solution (Thermo Fisher Scientific) and were kept at-80 <overline>C. Quantitative real time-PCR for MiR-181 and HOXA11 genes were performed. Results. MiR-181 expression level increased in eutopic tissue samples compared to the control group. This expression showed a significantly decrease in an ectopic group compared to the eutopic group. It was observed that HOXA11expression decreased remarkably in eutopic group compared to the control group and increased in ectopic group compared to the eutopic group. Conclusion. MiR-181 and HOXA11 are promising strategies in endometriosis disease. Understanding this relation and regulation roles contribute to realizing the etiology of endometriosis.
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页码:33 / 38
页数:6
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