KRT16 and APOA1: key regulators of proliferation and lipid metabolism in non-small cell lung cancer.

This study aimed to analyze the biological function of KRT16 and its interaction mechanism with apolipoprotein A1 (APOA1) in Non-Small Cell Lung Cancer (NSCLC). KRT16 expression and prognostic value in NSCLC were analyzed using the TCGA, GEPIA, and STRING databases. Functional impacts were assessed in A549 cells transfected with shKRT16 or APOA1 overexpression vectors. Gene/protein expression (RT-qPCR, Western blot), proliferation (MTT, EdU), cell cycle/apoptosis (flow cytometry), migration/invasion (Transwell), and lipid droplet accumulation (Oil Red O, Nile Red staining) were evaluated. The KRT16-APOA1 interaction was verified by co-immunoprecipitation, immunofluorescence, and GST pull-down assays. In NSCLC, KRT16 was up-regulated, and its high levels were associated with advanced tumor stage, lymph node metastasis, and poor prognosis. KRT16 levels were significantly elevated in patients aged 21-40 and were associated with infection. Knockdown of KRT16 or overexpression of APOA1 inhibited proliferation, induced cell cycle arrest, promoted apoptosis, and reduced the accumulation of lipid droplet in A549 cells. KRT16 promoted NSCLC cell proliferation, migration, and lipid droplet accumulation by directly interacting with APOA1. KRT16 is highly expressed in NSCLC and regulates the malignant behaviors of NSCLC cells by interacting with APOA1.