Hypoxia promotes ovarian cancer progression via lnc-DARS-AS1/miR-378a-5p/SLC2A12 axis

This study aimed to examine hypoxia-induced phenotypic alterations in ovarian cancer and to elucidate the molecular mechanisms mediated by long non-coding RNAs (lncRNAs). Transwell assay was used to assess migration and invasion, and methylthiazolyldiphenyl-tetrazolium bromide (MTT) assay was used to assess proliferation. Western blot analysis was conducted to evaluate the expression of factors associated with epithelial–mesenchymal transition (EMT). RNA sequencing was carried out to identify potential targets, and dual-luciferase and biotin-labeled microRNA (miRNA) pull-down assays were performed to identify interactions between these targets. Gain- and loss-of-function experiments were conducted to validate their effects. Hypoxia promoted the migration, invasion, and EMT of HO8910 and A2780 cells. Under hypoxic conditions, the expression of lncRNA-aspartyl-transfer RNA synthetase antisense RNA 1 (lnc- DARS-AS1 ) was significantly increased, and this upregulation exerted a proliferative effect on ovarian cancer cells. Furthermore, lnc- DARS-AS1 promoted solute carrier family 2 member 12 (SLC2A12) expression, accelerating ovarian cancer progression. Luciferase, biotin-labeled miRNA pull-down, and cellular function assays confirmed that lnc- DARS-AS1 binds to miR-378a-5p to enhance SLC2A12 levels. The expression levels of SLC2A12 were determined in samples from patients with ovarian cancer, and they showed a positive correlation with cancer progression. This research established that the lnc- DARS-AS1 /miR-378a-5p/SLC2A12 axis is involved in ovarian cancer progression under hypoxic conditions, providing new perspectives on the treatment and management of ovarian cancer.