Lnc-THAP7-AS1 suppresses the ovarian cancer progression by targeting miR-92b-5p/fatty acid 2-hydroxylase signal axis.

BACKGROUND

Ovarian cancer (OC) ranks among the most lethal gynecological malignancies. Research has highlighted long noncoding RNAs (lncRNAs) as promising novel molecular targets for cancer therapy. This study endeavors to identify novel lncRNAs, elucidate their specific roles, and unravel their regulatory mechanism in OC development.

METHODS

Utilizing LncRNA Microarray technology, we screened for differentially expressed RNAs, ultimately selecting THAP7-AS1 for in-depth investigation. RNA pull-down, luciferase assays and FISH were performed to validate the interaction among THAP7-AS1, miR-92b-5p and FA2H. qRT-PCR was conducted to assess the expression of THAP7-AS1, miR-92b-5p and FA2H in OC tissues and cell lines. Cellular biological effects were examined using proliferation CCK-8 and EdU assays, chamber Transwell migration assays, and flow cytometer for apoptosis analysis. Additionally, nude mice xenograft models were established to evaluate the in vivo effect of THAP7-AS1 on tumor growth.

RESULTS

Our findings revealed a downregulation of THAP7-AS1 in OC tissues and cells. Overexpression of THAP7-AS1 inhibited cell proliferation, migration, and induced apoptosis. miR-92b-5p was identified as a sponge target of THAP7-AS1, with its expression upregulated in OC tissues and cells. Forced expression of miR-92b-5p exhibited cellular effects opposite to those of THAP7-AS1 overexpression. Additionally, FA2H was confirmed as a direct target of miR-92b-5p Silencing FA2H suppressed apoptosis, promoted proliferation and migration. In vivo experiments showed overexpression of THAP7-AS1 significantly reduced tumor volume and weight.

CONCLUSION

THAP7-AS1 is firstly reported as a tumor suppressor in OC by targeting the miR-92b-5p/FA2H axis. Our findings suggest that THAP7-AS1 holds potential as therapeutic target in OC treatment.