LINC01198 activates Hippo signaling to stimulate IL-1β autocrine for driving vemurafenib resistance by associating with TAOK1/2 in melanoma.

ABSTRACT: Vemurafenib (VEM) is an important targeted drug for treating melanoma harboring BRAF-V600E mutation. Despite its remarkable curative efficacy in early clinical treatment, most patients developed drug resistance within one year. Nevertheless, the critical factors driving vemurafenib resistance and mechanisms leading to treatment failure in melanoma are debating and inconclusive. In this study, we established vemurafenib-resistance melanoma cell strain together with acute vemurafenib treatment and characterized LINC01198 as the only one LncRNA up-regulated in both of stable vemurafenib-resistant and acute vemurafenib-treated melanoma cells. Functionally, loss of LINC01198 significantly compromised melanoma resistance against vemurafenib. Mechanistically, LINC01198 directly associates with TA

SUBMITTER: Liu J 

PROVIDER: S-EPMC12559216 | biostudies-literature | 2025 Oct

REPOSITORIES: biostudies-literature