DNAJC12 activated by HNF1A enhances aerobic glycolysis and drug resistance in non-small cell lung cancer.

ABSTRACT:

Background

The DnaJ heat shock protein family member C12 (DNAJC12) gene has been demonstrated to promote lung cancer cell growth and migration by increasing β‑catenin expression. In this study, we aimed to reveal the role of DNAJC12 in modulating aerobic glycolysis and cisplatin (DDP) resistance in non-small cell lung cancer (NSCLC).

Methods

Bioinformatics analysis was applied to assess the expression levels of DNAJC12 and hepatocyte nuclear factor 1-alpha (HNF1A) in NSCLC tissues and the correlation between DNAJC12 and HNF1A expression levels. Cell Counting Kit-8 (CCK-8), flow cytometry assay, and in vivo tumor formation were used to evaluate cell growth, apoptosis, and tumorigenesis. Luciferase gene reporter assay was adopted to as

SUBMITTER: Wang J 

PROVIDER: S-EPMC9096394 | biostudies-literature | 2022 Apr

REPOSITORIES: biostudies-literature