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Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics
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Propofol Inhibits the Stem Characteristics and Tumor Growth of NSCLC by Altering the Expression and Localization of

Mei Liu1, Hongxia Leng2, Jiawei Wang2

  • 1Department of Anesthesiology and Operation, Medical Center of Anesthesiology and Pain, the First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, China.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|December 22, 2025
PubMed

Insights

Propofol inhibits non-small cell lung cancer (NSCLC) stemness and growth by regulating HDAC1 expression and miR-21-5p levels. This offers new therapeutic strategies for advanced NSCLC treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Advanced non-small cell lung cancer (NSCLC) often exhibits drug resistance, driven by cancer stem cells.
  • Histone deacetylase 1 (HDAC1) and ARID1A are implicated in tumor progression, particularly in EGFR-mutated NSCLC.

Purpose of the Study:

  • To investigate the role of HDAC1 in propofol's antitumor effects in NSCLC.
  • To elucidate the molecular mechanisms underlying propofol's impact on NSCLC stemness and growth.

Main Methods:

  • Utilized NSCLC cell lines (A549, HCC827) and nude mouse models.
  • Assessed propofol's effects on cancer stem cell markers (CD133, CD44, ABCG2, ALDH1A1).
  • Investigated propofol's influence on HDAC1 and ARID1A enrichment, H3K27 deacetylation, and miR-21-5p levels.

Main Results:

  • Propofol inhibited NSCLC cell stemness, proliferation, migration, invasion, and tumor growth.
  • Propofol downregulated key stem cell markers and promoted HDAC1/ARID1A enrichment at the ALDH1A1 promoter, repressing ALDH1A1 transcription.
  • Propofol inhibited HDAC1 expression and miR-21-5p levels; HDAC1 overexpression reversed these effects.

Conclusions:

  • Propofol exerts antitumor effects in NSCLC by inhibiting stem characteristics and tumor growth.
  • The mechanism involves regulating HDAC1 expression and translocation, leading to decreased miR-21-5p and subsequent tumor inhibition.
  • Propofol presents potential therapeutic targets and strategies for advanced NSCLC.
Keywords:
HDAC1NSCLCcancer stem genesmiR‐21‐5ppropofol

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