SNX17 mediates STAT3 activation to promote hepatocellular carcinoma progression via a retromer dependent mechanism.

ABSTRACT: Endocytosis has emerged as a key regulator of malignant behavior in cancer. Members of the sorting nexin (SNX) family have been found to be dysregulated in various cancers and play significant roles in regulating tumor metastasis. However, the role and mechanism of SNX17 in hepatocellular carcinoma (HCC) progression remain largely unknown. Here, we found that upregulation of SNX17 in HCC was associated with poor prognosis. Overexpression of SNX17 promoted HCC cell proliferation, migration, invasion, and metastasis, whereas silencing SNX17 expression resulted in opposite effects. Knockdown of SNX17 induced G1/S phase arrest and apoptosis. We discovered that SNX17 directly interacted with STAT3 and increased its phosphorylation in a retromer-dependent manner. SNX17-retromer complex acted as

SUBMITTER: Liu Y 

PROVIDER: S-EPMC12035908 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature