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KAT6A Promotes Lung Cancer Proliferation and Invasion via Keap1-Nrf2 Signaling.

Qian Ning1, Weichao Bai2, Hong Li1

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Advanced Biology
|May 4, 2026
PubMed
Summary

Lysine acetyltransferase 6A (KAT6A) promotes lung cancer progression by enhancing Nrf2 signaling and regulating oxidative stress. High KAT6A expression correlates with advanced lung adenocarcinoma and poorer survival, suggesting its potential as a prognostic biomarker.

Keywords:
KAT6A (histone acetyltransferase)Keap1‐Nrf2 pathwaylung canceroxidative stress

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Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Lung cancer remains a leading cause of cancer mortality worldwide.
  • Understanding the molecular mechanisms driving lung cancer progression is crucial for developing effective therapies.
  • The role of lysine acetyltransferase 6A (KAT6A) in lung cancer and its connection to oxidative stress pathways, particularly Nrf2, require further investigation.

Purpose of the Study:

  • To elucidate the function of KAT6A in lung adenocarcinoma progression.
  • To investigate the involvement of KAT6A in regulating Nrf2-mediated oxidative stress.
  • To assess KAT6A as a potential prognostic biomarker for lung adenocarcinoma.

Main Methods:

  • KAT6A was overexpressed and silenced in lung cancer cell lines (A549, H1299).
  • Quantitative reverse transcription polymerase chain reaction and Western blot were used to verify KAT6A expression.
  • Cell proliferation, invasion, oxidative stress markers (ROS, MDA, SOD), protein interactions (co-immunoprecipitation), and transcriptional activity (dual-luciferase reporter assays) were assessed.
  • Immunohistochemistry was performed on clinical lung adenocarcinoma samples.

Main Results:

  • KAT6A overexpression promoted lung cancer cell proliferation and invasion, while silencing suppressed these effects.
  • KAT6A overexpression decreased Keap1, enhanced Nrf2 signaling, reduced reactive oxygen species (ROS) and malondialdehyde (MDA) levels, and increased superoxide dismutase (SOD) activity.
  • KAT6A directly interacted with Nrf2, enhancing its transcriptional activity on the heme oxygenase-1 promoter.
  • Silencing Nrf2 reversed the pro-proliferative effects of KAT6A.
  • High KAT6A expression in clinical samples correlated with advanced tumor stage and reduced overall survival.

Conclusions:

  • KAT6A promotes lung adenocarcinoma malignant progression by modulating the Keap1-Nrf2 pathway and regulating oxidative stress.
  • KAT6A may serve as a valuable prognostic biomarker for lung adenocarcinoma, indicating potential therapeutic targets.