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Mechanical regulation of adipogenic reprogramming suppresses ovarian cancer progression

Yu-Huan Li1, Jia-Wen Zhao1,2,3, Xin Wang2,3,4

  • 1Maternity Center, First Hospital of Jilin University, Changchun, Jilin, China.

Communications Biology
|June 29, 2026
PubMed

Insights

Reprogramming ovarian cancer cells into adipocytes using (‒)-Blebbistatin and adipogenic stimuli halts tumor growth. This cytoskeletal destabilization approach offers a novel differentiation-targeted therapy for epithelial ovarian cancer (EOC).

Area of Science:

  • Oncology
  • Cell Biology
  • Biochemistry

Background:

  • Epithelial ovarian cancer (EOC) is a deadly malignancy with frequent recurrence due to chemoresistance and micrometastases.
  • Cytoskeletal regulation is explored as a novel therapeutic strategy to alter cancer cell fate.

Purpose of the Study:

  • To investigate the potential of combining cytoskeletal destabilization with adipogenic stimuli to induce transdifferentiation of EOC cells.
  • To elucidate the underlying mechanisms of this reprogramming and its therapeutic implications.

Main Methods:

  • Ovarian cancer cells were treated with (‒)-Blebbistatin (Ble) and adipogenic stimuli (BMP4 or PPARγ agonists) in vitro and in vivo.
  • Tumor growth suppression was assessed in subcutaneous and intraperitoneal models.
  • Mechanistic studies involved analyzing lipid droplet accumulation, adipogenic marker expression, chromatin remodeling, and mechanical signaling pathways (YAP).

Main Results:

  • The combination treatment effectively induced adipogenic transdifferentiation of EOC cells, characterized by lipid accumulation and upregulated adipogenic markers.
  • Transformed cells exhibited functional lipolysis and tumor growth suppression in preclinical models.
  • Cytoskeletal destabilization was shown to trigger heterochromatin redistribution, enhancing transcription factor accessibility and promoting adipogenesis, with YAP signaling playing a critical role.

Conclusions:

  • Cytoskeletal destabilization combined with adipogenic cues can reprogram EOC cells into adipocyte-like cells via heterochromatin remodeling.
  • This differentiation-targeted approach shows promise for overcoming EOC recurrence and chemoresistance.
  • The findings provide preclinical evidence for a novel therapeutic strategy in ovarian cancer treatment.

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