CircATRNL1 increases acid-sensing ion channel 1 to advance epithelial-mesenchymal transition in endometriosis by binding to microRNA-103a-3p

Xiyun Chen, Min Liu
Reproductive biology · 2022 · vol. 22(2) , pp. 100643 · doi:10.1016/j.repbio.2022.100643 · PMID:35504053 · W4229066374
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CircATRNL1 upregulates acid-sensing ion channel 1 by sponging microRNA-103a-3p, thereby promoting epithelial-mesenchymal transition in endometriosis.

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Abstract

Circular RNA ATRNL1 (circATRNL1) has been implicated in epithelial-mesenchymal transition (EMT) during endometriosis. Given the existing literature and our predictions through starBase in this research, it was assumed that circATRNL1 might orchestrate the microRNA (miR)- 103a-3p/acid-sensing ion channel 1 (ASIC1) axis to control EMT in endometriosis. To verify our hypothesis, we detect circATRNL1, miR-103a-3p, and ASIC1 expression in endometrial cancer cells (HEC-B, AN3-CA, KLE, HEC1-A, and Ishikawa). Ishikawa cells with the highest circATRNL1 level were selected as subjects, where circATRNL1, miR-103a-3p, or ASIC1 expression was knocked down. Scratch and Transwell assays were applied to assess cell migration and invasion, and CCK-8 and colony formation assays to detect cell proliferation. Western blot was used to measure E-cadherin, N-cadherin, Vimentin, and Slug expression to evaluate the EMT state. Furthermore, the binding of miR-103a-3p to circATRNL1 or ASIC1 was validated by luciferase reporter assay. CircATRNL1 and ASIC1 were upregulated but miR-103a-3p was downregulated in endometrial cancer cells. Mechanistically, circATRNL1 bound to miR-103a-3p to upregulate a target gene of miR-103a-3p, ASIC1. CircATRNL1 silencing contributed to the decline of proliferation, invasion, migration, and EMT in Ishikawa cells, while miR-103a-3p inhibitor reversed those changes. In addition, the EMT process was aggravated when miR-103a-3p was inhibited and this process was suppressed by silencing ASIC1 in the presence of downregulated miR-101a-3p. Our study supported that circATRNL1 might be a novel therapeutic candidate target for endometriosis treatment and provided unique insights into the molecular basis concerning the pathogenesis of endometriosis.

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Condition tags

endometriosis

MeSH descriptors

Endometrial Neoplasms Endometrial Neoplasms Endometrial Neoplasms Endometrial Neoplasms Endometrial Neoplasms Endometrial Neoplasms Endometrial Neoplasms Endometrial Neoplasms Endometrial Neoplasms Endometrial Neoplasms Endometrial Neoplasms Endometrial Neoplasms Endometrial Neoplasms Endometrial Neoplasms Endometrial Neoplasms Endometrial Neoplasms Endometrial Neoplasms Endometrial Neoplasms Endometrial Neoplasms Endometrial Neoplasms

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