The role of HOTAIR/miR-152-3p/LIN28B in regulating the progression of endometrial squamous carcinoma

Introduction: There is growing evidence that long non-coding RNAs (lncRNAs) are correlated with malignancy in the modulation of tumor progression. This study aims to investigate the effect of homeobox protein (HOX) transcript antisense RNA (HOTAIR) on the migration and invasion of ESC. Material and methods: Starbase was used to identify miRNAs with complementary base pairing with HOTAIR. RNA pull-down and qRT-PCR were employed to investigate the effect of HOTAIR on miR-152-3p. In vitro cell migration and invasion assays were performed to assess the effects of HOTAIR and miR-152-3p on ESC. Computational software, TargetScan, was then used to identify the potential target of miR-152-3p, and their relationship was verified by immunoblotting analysis, qRT-PCR and luciferase reporter assay. Results: Starbase predicted a potential miR-152-3p binding site in HOTAIR, which was validated by RNA pull-down assay. HOTAIR was negatively correlated with miR-152-3p in ESC. Moreover, HOTAIR promoted migration and invasion of ESC. The oncogenic activity of HOTAIR was partly through its negative regulation of miR-152-3p. LIN28B was identified to be a direct target of miR-152-3p. A negative correlation between LIN28B and miR-152-3p was observed in ESC. In addition, overexpression of miR-152-3p suppressed the progression of ESC by directly targeting and regulating LIN28B. Conclusions: Our results reveal that HOTAIR may be a driver of ESC through inhibiting miR-152-3p, a tumor suppressor, suggesting that miR-152-3p may be a potential target for advanced ESC therapeutic treatment.

Automated summary

This study demonstrates that HOTAIR promotes the migration and invasion of ESC by inhibiting miR-152-3p, suggesting miR-152-3p as a potential therapeutic target for advanced ESC treatment. Additionally, LIN28B was identified as a direct target of miR-152-3p, with a negative correlation observed between LIN28B and miR-152-3p in ESC. Overexpression of miR-152-3p suppressed ESC progression by regulating LIN28B.