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p53 Drives Lung Cancer Regression through a TSC2/TFEB-dependent Senescence Program.

Mengxiong Wang1, Kathryn T Bieging-Rolett1, Alyssa M Kaiser1

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|October 20, 2025
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Summary
This summary is machine-generated.

Restoring tumor suppressor p53 function can fight lung adenocarcinoma (LUAD). This study reveals p53 triggers senescence and macrophage recruitment, leading to tumor regression and offering new therapeutic targets.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Pharmacological restoration of p53 tumor suppressor function is a promising strategy for cancers like lung adenocarcinoma (LUAD).
  • The p53 pathway's complexity and potential toxicity have hindered its therapeutic application.
  • Understanding the precise mechanisms of p53-mediated responses is crucial for developing effective treatments.

Purpose of the Study:

  • To deconstruct the transcriptional programs and downstream effects of p53 in LUAD.
  • To identify key molecular events driving therapeutic responses and tumor regression.
  • To illuminate potential targets for optimizing p53-based combination therapies.

Main Methods:

  • Utilized both mouse and human models of LUAD.
  • Analyzed transcriptional programs and cellular sequelae following p53 activation.
  • Investigated the roles of Tsc2, mTORC1, TFEB, autophagy, senescence, and macrophage recruitment.

Main Results:

  • p53 directly transactivates Tsc2, inhibiting mTORC1 and promoting TFEB nuclear accumulation.
  • This cascade induces lysosomal gene expression, autophagy, and cellular senescence in LUAD cells.
  • Senescent cells recruit macrophages, leading to phagocytosis and tumor regression.

Conclusions:

  • A complex cascade of events underlies p53 therapeutic responses in LUAD.
  • Targetable nodes within this cascade offer opportunities for combination therapies.
  • This framework is critical for optimizing p53-based therapeutics in LUAD.