Targeting CREB3L2-mediated lipid metabolism overcomes lenvatinib resistance and attenuates the progression of hepatocellular carcinoma.

ABSTRACT: When hepatocellular carcinoma (HCC) cells exhibit malignant biological behaviors, lipid metabolic reprogramming occurs concomitantly. Thus, identifying regulators of metabolic reprogramming offers new potential targets for therapy. In this study, we investigated the mechanisms by which Cyclic adenosine monophosphate-responsive element binding protein 3-like 2(CREB3L2) influences HCC progression and contributes to lenvatinib resistance through modulation of lipid metabolism. Up-regulated expression of CREB3L2 was observed in numerous HCC cohorts and associated with poor survival prognosis of patients. Furthermore, CREB3L2 could facilitate the proliferation and metastatic capacity of HCC cells both in vitro and in vivo. It was found that CREB3L2 influences the proliferation and metastasis of

SUBMITTER: Yang S 

PROVIDER: S-EPMC12644697 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature