Correlation Between microRNA-let-7a and microRNA-10b Expression and KRAS and E-Cadherin Gene Expression in the Endometrium of Patients with Adenomyosis

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Wahyuni Saddang, Muharam, Mila Maidarti, Kanadi Sumapraja, Gita Pratama, Rizka Yurianda

Abstract

Adenomyosis is a common benign gynecological disorder associated with chronic pelvic pain and infertility, for which current treatments are limited to symptom relief and are often unsuitable for women seeking pregnancy. Altered E-cadherin expression and dysregulation of microRNAs, including let-7a and miR-10b, have been implicated in adenomyosis pathogenesis, but their relationship with the proposed target genes KRAS and E-cadherin has not been well characterized in this condition. This cross-sectional study compared the relative expression of miRNA-let-7a, miR-10b, KRAS, and E-cadherin in endometrial tissue from women with adenomyosis (n=17) and without adenomyosis (n=15) recruited at Dr. Cipto Mangunkusumo Hospital, Jakarta [AUTHOR VERIFICATION REQUIRED: total analytical sample], and examined the associations between miRNA-let-7a and KRAS, and between miR-10b and E-cadherin, using quantitative PCR and Pearson correlation. E-cadherin expression was significantly lower in the adenomyosis group than in the non-adenomyosis group (0.39 vs 1.36; p=0.001). No significant between-group differences were found for miRNA-let-7a (p=0.288), miR-10b (p=0.320), or KRAS (p=0.509). miRNA-let-7a showed a weak negative correlation with KRAS in the non-adenomyosis group (r=-0.287, p=0.300) but not in the adenomyosis group (r=0.024, p=0.926). miR-10b showed weak-to-moderate negative correlations with E-cadherin in both groups, neither statistically significant (adenomyosis: r=-0.147, p=0.572; non-adenomyosis: r=-0.350, p=0.201). These findings support an association between reduced E-cadherin expression and adenomyosis but do not establish a direct regulatory relationship between the investigated microRNAs and their proposed target genes. Larger, molecularly stratified studies with functional validation are warranted.

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