Related Experiment Video

Updated: Jan 25, 2026

Anticancer Efficacy of Photodynamic Therapy with Lung Cancer-Targeted Nanoparticles
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Published on: December 1, 2016

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YAP inhibition by gloriosine unlocks autophagic cell death as an anticancer strategy in lung malignancies

Biswajit Dey1, Bharat Goel2, Essha Chatterjee1

  • 1Department of Biological Sciences, National Institute of Pharmaceutical Education and Research, Balanagar, 500037, Hyderabad, India; Department of Biotechnology and Bioinformatics, Sambalpur University, Jyoti Vihar, Burla, Sambalpur, 768019, Odisha, India.

European Journal of Pharmacology
|January 23, 2026
PubMed

Insights

Gloriosine shows promise as a new lung cancer therapy, selectively reducing cancer cell viability and tumor size while sparing normal cells. It works by arresting the cell cycle and impacting key signaling pathways.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Lung cancer remains a leading cause of cancer death globally.
  • Current therapies face challenges with drug resistance, toxicity, and limited efficacy.
  • Novel chemotherapeutic agents are needed to improve treatment outcomes.

Purpose of the Study:

  • To investigate the anticancer potential of the isolated compound, gloriosine.
  • To evaluate gloriosine's efficacy and mechanism of action against A549 lung adenocarcinoma cells.
  • To assess gloriosine's safety profile on normal cells.

Main Methods:

  • In vitro cell viability assays on various cancer cell lines, including A549.
  • In vivo tumor xenograft studies to assess tumor size reduction.
  • Cell cycle analysis and Western blotting to elucidate molecular mechanisms, focusing on the Hippo and AKT/mTOR pathways.

Main Results:

  • Gloriosine significantly reduced cancer cell viability and tumor size in a dose- and time-dependent manner.
  • Gloriosine demonstrated selective cytotoxicity, with minimal impact on normal cells.
  • Mechanistically, gloriosine induced G2/M cell cycle arrest, inhibited the Hippo-YAP pathway, suppressed AKT/mTOR signaling, and activated autophagy-dependent cell death.

Conclusions:

  • Gloriosine exhibits potent and selective anticancer activity against lung adenocarcinoma.
  • The compound's mechanism involves cell cycle arrest and modulation of critical signaling pathways.
  • Gloriosine represents a promising candidate for developing novel lung cancer therapeutics.
Keywords:
AKT/mTOR pathwayAutophagyCell deathG2/M cell cycle arrestGloriosineHippo signaling

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