Lnc‐RNA LINC01279 induces endometriosis via targeting of HOXA10. Issue 5 (3rd March 2021) - Liu, Liling
Abstract: Aim: To explore the regulatory role and molecular mechanism of lncRNA‐LINC01279 in endometriosis (EMs). Methods: Between September 2018 and July 2019, 20 EMs patients and 20 healthy subjects were recruited to detect the expression of lncRNA‐LINC01279 in EMs and in normal endometrium via qRT‐PCR. Autograft was used to establish EMs models on Spraque–Dawley (SD) rats, which was followed by taking volume measurements of EMs endometrium and observing pathological changes in the morphology of EMs via hematoxylin and eosin (H&E) staining. The qRT‐PCR technique was further carried out to determine mRNA expression of lncRNA‐LINC01279 and HOXA10 in the serum of EMs rats and LINC01279 shRNA‐transfected rats, while the protein expression of HOXA10 was determined using a Western blot. Results: EMs patients presented with upregulation of lncRNA‐LINC01279 and downregulation of HOXA10 ( p < 0.01 or 0.001). Online predictions further revealed that lncRNA‐LINC01279 regulated the expression of HOXA10 via miRNA‐135b. In EMs models, it was observed that there were a significantly enlarged endometrium and poor pathological morphology, significant upregulation of lncRNA‐LINC01279, and downregulation of miR‐135b and HOXA10 in serum ( p < 0.05, 0.01 or 0.001). In the lncRNA‐LINC01279 shRNA group, EMs rats, following treatment, had a sharp decrease in the volume of EMs endometrium, and an improvement in pathological morphology, while lncRNA‐LINC01279 was downregulated, with upregulation of miR‐135b and HOXA10 ( p < 0.05, 0.01 or 0.001). Conclusion: LncRNA‐LINC01279, by the mechanism of targeting miR‐135b, has the potential to downregulate the expression of HOXA10, and therefore, can promote the development and progression of EMs.