PulseExploreJournal ClubDebatesTrendingResearchersJournals
Instagram
HomeExploreJournal ClubTrending
Synapse
⌘+K
Synapse
April 11, 2026Acta Biochimica et Biophysica SinicaOpen Access

Genetic mutation and dysfunction of AT2 cells drive B(a)P/LPS-induced inflammation-related lung tumorigenesis: evidence and mechanism of autophagy

View Full Paper
Ask AI
Bookmark
Share

Authors

ZTZhihao Gavin TangXZXianchao ZhouPSPingping Shang

Discussion

Loading...

Member takes

Overview

Novel insights reveal altered AT2 cell function and increased inflammation-related tumorigenesis in mice exposed to pollutants.

Key Points

  • To investigate the genetic mutations and functional changes in AT2 cells that drive inflammation-related lung tumorigenesis.
  • Exposed C57BL/6J mice to B(a)P and LPS to model inflammation-related lung tumorigenesis.
  • Performed single-cell RNA sequencing on lung tissues to analyze gene expression.
  • Conducted whole-exome sequencing to study DNA mutations in AT2 cells.
  • Used immunofluorescence staining to evaluate protein expression in AT2 cells.
  • LPS exposure enhances B(a)P-induced lung tumorigenesis in mice.
  • AT2 cells exhibited decreased proportions and altered differentiation trajectories.
  • Increased DNA mutations and levels of γ-H2AX and Ki67 were observed in AT2 cells post-treatment.
  • Autophagy-related genes in AT2 cells are significantly downregulated in B(a)P/LPS-treated lung cancer tissue.

Cite This Study

Tang et al. (2026) studied this question.

synapsesocial.com/papers/69d9e67a78050d08c1b76e91https://doi.org/10.3724/abbs.2025238
View Full Paper
Ask AI
Bookmark
Share