RESUMO
BACKGROUND: Reportedly, ovarian cancer (OC) is a major threat to women's health. Long non-coding RNA (lncRNA) ASB16-AS1 has been uncovered to participate in cancer progression. Nevertheless, the role of ASB16-AS1 in OC remains to be revealed. PURPOSE: This study aimed to unveil the biological function of ASB16-AS1 and its underlying mechanisms in OC cells. METHODS: QRT-PCR was done to test ASB16-AS1 expression in OC cells. Functional assays were performed to evaluate the malignant behaviors and cisplatin resistance of OC cells. Mechanistic analyses were done to investigate the regulatory molecular mechanism in OC cells. RESULTS: ASB16-AS1 was found to be highly expressed in OC cells. ASB16-AS1 knockdown repressed proliferation, migration, and invasion of OC cells, while facilitating cell apoptosis. ASB16-AS1 was further validated to up-regulate GOLM1 through competitively binding with miR-3918. Moreover, miR-3918 overexpression was corroborated to suppress OC cell growth. Rescue assays further uncovered that ASB16-AS1 modulated the malignant processes of OC cells via targeting miR-3918/GOLM1 axis. CONCLUSION: ASB16-AS1 facilitates the malignant processes and chemoresistance of OC cells via serving as miR-3918 sponge and positively modulating GOLM1 expression.