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Updated: Apr 8, 2026

An Orthotopic Bladder Cancer Model for Gene Delivery Studies
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Apigenin Suppresses Bladder Cancer via the SIRT6-NCOA2-PPARα Axis

Ying Liu1,2, Zhen-Duo Shi1,2,3, Yun-Fei Wei4,5

  • 1School of Life Sciences, Jiangsu Normal University, Xuzhou, China.

International Journal of Biological Sciences
|April 7, 2026
PubMed

Insights

Apigenin, a natural compound, suppresses bladder cancer by enhancing SIRT6-mediated deacetylation of NCOA2. This action reprograms cellular metabolism, revealing a new therapeutic target for bladder cancer treatment.

Area of Science:

  • Oncology
  • Biochemistry
  • Molecular Biology

Background:

  • Protein acetylation regulates tumor progression, but natural modulators are unclear.
  • Dietary flavonoids like apigenin show potential in cancer therapy.
  • Understanding molecular mechanisms is crucial for developing targeted treatments.

Purpose of the Study:

  • To investigate the role of apigenin in bladder cancer progression.
  • To elucidate the molecular mechanisms underlying apigenin's anti-cancer effects.
  • To identify novel therapeutic targets in bladder cancer.

Main Methods:

  • In vitro functional assays and dynamic xenograft models were used.
  • An integrated multi-omics approach was applied.
  • SIRT6-mediated deacetylation of Nuclear Receptor Coactivator 2 (NCOA2) was analyzed.

Main Results:

  • Apigenin enhances SIRT6-mediated deacetylation of NCOA2 at specific lysine residues (780 and 785).
  • This modification potentiates PPARα activity, reprograms cellular metabolism, and disrupts mitochondrial function.
  • Reduced SIRT6 and elevated NCOA2 correlate with metastatic bladder cancer.

Conclusions:

  • A novel SIRT6-NCOA2-PPARα signaling axis is identified in bladder cancer.
  • This axis represents a metabolic vulnerability exploitable for therapeutic intervention.
  • Apigenin's mechanism offers a potential strategy for bladder cancer treatment.
Keywords:
NCOA2SIRT6apigeninbladder cancermetabolic reprogramming

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