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Panobinostat inhibits breast cancer progression via Vps34-mediated exosomal pathway

Xuan Wang1, Xuzhi Yin2

  • 1Department of Pharmacology, School of Basic Medicine Qingdao University, 308 Ningxia Road, Qingdao, 266071, China. wx105yxz@163.com.

Human Cell
|November 4, 2022
PubMed

Insights

Panobinostat (LBH589), an HDAC inhibitor, promotes breast cancer cell exosome release via the Vps34/Rab5C pathway, inhibiting tumor progression. This reveals a novel exosome-mediated anti-tumor mechanism for LBH589.

Area of Science:

  • Oncology
  • Cell Biology
  • Pharmacology

Background:

  • Exosomes mediate intercellular communication and are implicated in tumor metastasis.
  • Histone deacetylase (HDAC) inhibitors, like Panobinostat (LBH589), show anti-tumor potential.
  • Exosomes can transfer drugs between cells, influencing therapeutic outcomes.

Purpose of the Study:

  • To investigate if Panobinostat (LBH589) regulates tumor growth through exosome secretion.
  • To elucidate the mechanism by which LBH589 affects exosome release and function in breast cancer.

Main Methods:

  • Induction of autophagy and secretory autophagy by LBH589.
  • Assessment of LBH589-stimulated exosome release via the Vps34/Rab5C pathway.
  • Experimental ablation of Vps34 and/or Rab5C in breast cancer cells to confirm pathway involvement.

Main Results:

  • LBH589 treatment induced autophagy and facilitated secretory autophagy.
  • LBH589 dose- and time-dependently stimulated exosome release, mediated by the Vps34/Rab5C pathway.
  • LBH589 demonstrated inhibition of breast cancer progression through exosome-mediated effects.

Conclusions:

  • A novel mechanism of LBH589's anti-tumor activity in breast cancer involves exosome secretion.
  • LBH589 utilizes the Vps34/Rab5C pathway to enhance exosome release, contributing to cancer suppression.
  • This study highlights the role of exosomes in mediating the therapeutic effects of LBH589.
Keywords:
Breast cancer progressionExosomePanobinostatSecretory autophagyVps34

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