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Baicalein upregulates DDIT4 expression which mediates mTOR inhibition and growth inhibition in cancer cells

Yujun Wang1, Ernest Han1, Quanhua Xing1

  • 1Departments of Surgery, Beckman Research Institute of City of Hope, 1500 E. Duarte Rd, Duarte, CA 91010, USA.

Cancer Letters
|December 29, 2014
PubMed

Insights

Baicalein, a natural compound, boosts DDIT4 expression, inhibiting mTORC1 signaling and cancer cell growth. This mechanism shows promise for cancer treatment and prevention, even in drug-resistant cells.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Cancer Research

Background:

  • Baicalein is a natural flavone with known anticancer properties.
  • The molecular mechanisms underlying baicalein's anticancer effects require further elucidation.
  • Identifying key molecular targets is crucial for developing novel cancer therapies.

Purpose of the Study:

  • To investigate the molecular targets of baicalein in cancer cells.
  • To determine the role of DDIT4 (DNA-Damage Inducible Transcript 4) in baicalein's anticancer activity.
  • To explore the potential of baicalein as a therapeutic agent for cancer, including platinum-resistant cancers.

Main Methods:

  • Microarray analysis to identify baicalein-induced transcripts.
  • Quantitative RT-PCR and immunoblotting to confirm DDIT4 expression.
  • Cell culture experiments with various cancer cell lines, including p53 knockout cells.
  • RNA interference to assess the role of DDIT4.
  • In vivo studies using a mouse model of breast cancer.
  • Assessment of mTORC1 (mammalian Target of Rapamycin Complex 1) activity through phosphorylation of its targets.

Main Results:

  • Baicalein significantly upregulates DDIT4 expression in a dose-dependent and time-dependent manner across multiple cancer cell lines.
  • DDIT4 induction by baicalein is independent of p53 status.
  • Baicalein suppresses mTORC1 activity, evidenced by decreased phosphorylation of mTORC1 targets.
  • Knockdown of DDIT4 attenuates baicalein-induced mTORC1 inhibition and growth inhibition.
  • Baicalein suppresses tumor growth in a mouse model, correlating with increased DDIT4 expression.
  • Baicalein effectively inhibits platinum-resistant cancer cells by upregulating DDIT4 and inhibiting mTORC1.

Conclusions:

  • Baicalein inhibits cancer cell growth and tumor progression by inducing DDIT4 expression, leading to mTORC1 pathway inhibition.
  • DDIT4 is a key mediator of baicalein's anticancer effects.
  • Baicalein represents a potential therapeutic strategy for cancer chemotherapy and chemoprevention, particularly for platinum-resistant malignancies.
Keywords:
BaicaleinCellular stressDDIT4IRF1mTOR

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