Long non‑coding RNA LINC01960‑201 hinders decidualization of endometrial stromal cell in endometriosis: Relevance to endometrial receptivity.

Emerging data have indicated that long non‑coding RNAs (lncRNA) are associated with the pathogenesis of endometriosis. However, few are associated with endometriosis‑associated infertility. In addition, to the best of our knowledge, the role of lncRNAs in decidual formation during the window of implantation with endometriosis has not been reported to date. Based on our previous results, the aim of the present study was to explore the role of lncRNA long intergenic non‑protein coding RNA (LINC)01960‑201 in in vitro decidualization of endometrial stromal cells in endometriosis during the window of implantation, as well as to explore the biological function of LINC01960‑201, and the regulation of a disintegrin and metalloproteinase with thrombospondin motifs 7 (ADAMTS7), hsa‑microRNA (miR)‑760 and hsa‑miR‑608 in the decidualization of endometrial stromal cells with endometriosis. Using miRanda, PITA and RNAhybrid, the present study predicted which miRs share the common target gene ADAMTS7 with LINC01960‑201 and the existence of regulatory targets. Dual luciferase vectors were constructed to extract the plasmids and measure the relative fluorescence values in order to estimate target regulatory association between LINC01960‑201, ADAMTS7 and miRs. Mid‑secretory endometrial tissues were collected from women with endometriosis‑associated infertility. From these tissues, endometrial stromal cells were extracted and cultured as primary cultures. Medroxyprogesterone acetate (MPA) and 8‑Bromoadenosine 3',5'‑cyclic monophosphate (8‑Br‑cAMP) were added to induce decidualization, and to knockdown LINC01960‑201 and transfect a hsa‑miR‑608 mimic at the same time. Reverse transcription‑quantitative PCR and western blotting were conducted to compare the difference in gene expression between the experimental and negative control groups. No regulatory sites between LINC01960‑201 and hsa‑miR‑608 were identified; however, potential regulatory sites were detected between hsa‑miR‑608 and the 3'‑untranslated region (UTR) of ADAMTS7, whereas neither the 3'‑UTR of LINC01960‑201 or the 3'‑UTR of ADAMTS7 had any regulatory targets with hsa‑miR‑760. During the process of decidualization of endometrial stromal cells by in vitro induction, the expression of hsa‑miR‑608 in the knockdown group was significantly higher compared with that of the negative control group after LINC01960‑201‑knockdown, and the expression of ADAMTS7 in the transfection group was significantly lower compared with that of the negative control group after hsa‑miR‑608 mimic transfection. In conclusion, it was hypothesized that LINC01960‑201 played a notable regulatory role in the decidualization of endometrial stromal cells in women with endometriosis during the window of implantation, and its abnormal expression may lead to the decline of endometrial receptivity and recurrent abortions.