BCAT1 promotes lung adenocarcinoma progression through enhanced mitochondrial function and NF-κB pathway activation

J Zhejiang Univ Sci B. 2022;23(9):760-769. doi: 10.1631/jzus.B2100985.

Abstract

Lung cancer is one of the most prevalent and malignant cancers, among which lung adenocarcinoma (LUAD) accounts for the majority and remains a major cause of cancer-related mortality worldwide (Cui et al., 2019). Despite the growing intensity of research on the pathobiology and progression of lung cancer and the fact that many genes have been identified as potential drivers and targets for therapy (Luo et al., 2019; Zhang et al., 2019), the treatment and prognosis of lung cancer patients have hardly improved. Therefore, this study aimed to investigate the precise mechanism of lung cancer development and explore efficient diagnostic and therapeutic methods for clinical treatment.

MeSH terms

  • Adenocarcinoma of Lung* / genetics
  • Adenocarcinoma of Lung* / pathology
  • Humans
  • Lung Neoplasms* / genetics
  • Lung Neoplasms* / pathology
  • Mitochondria / metabolism
  • NF-kappa B / metabolism
  • Transaminases*

Substances

  • NF-kappa B
  • BCAT1 protein, human
  • Transaminases