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Butein suppresses pancreatic cancer progression by downregulating CDK2 and disrupting CDK2/CyclinA2 interaction

Mengting Chen1, Xiaoyu Sun2, Yongjiang He1

  • 1School of Pharmacy, Hangzhou Normal University, Hangzhou, Zhejiang 311121, China.

Biochemical Pharmacology
|May 24, 2026
PubMed

Insights

Butein, a natural compound, effectively targets CDK2 to combat pancreatic cancer. It halts cell cycle progression, induces cell death, and inhibits tumor growth, offering a promising new therapeutic strategy.

Area of Science:

  • Oncology
  • Pharmacology
  • Molecular Biology

Background:

  • Pancreatic cancer is a deadly disease with few treatment options.
  • There is a critical need for novel therapeutic strategies.

Purpose of the Study:

  • To investigate butein as a potential anti-cancer agent for pancreatic cancer.
  • To identify the molecular target and mechanism of action of butein.

Main Methods:

  • In silico molecular docking
  • Cellular Thermal Shift Assay (CETSA)
  • Drug Affinity Responsive Target Stability (DARTS)
  • Cell cycle analysis
  • Apoptosis assays
  • Mouse xenograft models

Main Results:

  • Butein directly binds to and inhibits Cyclin-Dependent Kinase 2 (CDK2).
  • Butein induces G2/M cell cycle arrest, apoptosis, and inhibits proliferation.
  • Butein downregulates CDK2 expression and disrupts its interaction with cyclinA2.
  • CDK2 is essential for butein's anti-cancer effects; its knockdown synergizes with butein.
  • Butein significantly inhibits tumor growth in vivo without systemic toxicity.

Conclusions:

  • Butein is a potent CDK2 inhibitor with significant anti-tumor activity against pancreatic cancer.
  • Butein represents a promising therapeutic candidate for pancreatic cancer treatment.
  • Targeting CDK2 with butein offers a novel and translatable strategy for pancreatic cancer.
Keywords:
Anti-tumor activityButeinCDK2Natural productPancreatic cancer

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