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Updated: Apr 14, 2026

Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics
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A Novel Small-Molecule Inhibitor Targeting CREB-CBP Complex Possesses Anti-Cancer Effects along with Cell Cycle

Jong Woo Lee1, Hee Sun Park1, Sin-Aye Park1

  • 1Section of Medical Oncology, Department of Internal Medicine, Yale Comprehensive Cancer Center, Yale School of Medicine, Yale University, New Haven, CT 06520, United States of America.

Plos One
|April 22, 2015
PubMed

Insights

Naphthol AS-TR phosphate (NASTRp) inhibits lung cancer by halting cell cycle progression and suppressing tumor-promoting autophagy. This CREB-CBP inhibitor induces apoptosis, offering a potential new therapeutic strategy for lung adenocarcinoma.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Therapeutics

Background:

  • Lung adenocarcinoma is the most common and deadliest form of lung cancer globally.
  • Existing lung cancer treatments require novel therapeutic strategies to improve patient outcomes.

Purpose of the Study:

  • To investigate Naphthol AS-TR phosphate (NASTRp) as a potential therapeutic agent for lung adenocarcinoma.
  • To elucidate the molecular mechanisms underlying NASTRp's anti-cancer effects.

Main Methods:

  • Treatment of human lung cancer cell lines with NASTRp.
  • Analysis of cell cycle progression, autophagy markers (Atg5-12, Atg7, p62), endoplasmic reticulum stress markers (DDIT3/CHOP), and apoptosis markers (Bim).

Main Results:

  • NASTRp inhibited lung cancer cell proliferation by inducing cell cycle arrest.
  • NASTRp suppressed tumor-promoting autophagy through downregulation of Atg5-12 and Atg7, and p62 accumulation.
  • NASTRp induced endoplasmic reticulum stress and apoptosis via Bim induction.

Conclusions:

  • The cyclic-AMP response element-binding protein (CREB)-CREB binding protein (CBP) transcription factor complex is a viable therapeutic target in lung cancer.
  • NASTRp demonstrates potential as a novel therapeutic strategy for lung adenocarcinoma by targeting the CREB-CBP complex.

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