Long non-coding RNA ATP6V1B1-AS1 promotes ovarian cancer progression through targeting MAP3K3/p38 MAPK pathway

To explore the function and molecular mechanism of lncRNA ATP6V1B1-AS1 in ovarian cancer (OC). The expression pattern of ATP6V1B1-AS1 in OC was verified using TCGA database and RT-qPCR. CCK-8, colony formation and migration assays were applied to evaluate cell proliferation and migration after ATP6V1B1-AS1 silencing. Xenograft and lung metastasis models in nude mice were used for in vivo functional verification. RNA pull-down combined with LC-MS/MS was used to screen interacting proteins, which were further validated by co-immunostaining and Western blot. Western blot and rescue assays were performed to clarify the ATP6V1B1-AS1/MAP3K3/p38 MAPK signaling axis. ATP6V1B1-AS1 was upregulated in OC and correlated with poor patient prognosis. Silencing ATP6V1B1-AS1 suppressed the proliferation, migration, tumorigenesis and metastasis of OC cells. Mechanistically, ATP6V1B1-AS1 directly interacted with MAP3K3, and this interaction facilitated p38 MAPK phosphorylation to drive OC progression. LncRNA ATP6V1B1-AS1 accelerates OC progression via binding MAP3K3 and activating the p38 MAPK pathway. This work may provide a potential therapeutic target for OC.