4.5 Article

Valproic acid Suppresses Breast Cancer Cell Growth Through Triggering Pyruvate Kinase M2 Isoform Mediated Warburg Effect

期刊

CELL TRANSPLANTATION
卷 30, 期 -, 页码 -

出版社

SAGE PUBLICATIONS INC
DOI: 10.1177/09636897211027524

关键词

Warburg effect; Valproic acid; pyruvate kinase M2 isoform; histone deacetylases; cell proliferation; breast cancer

资金

  1. Startup Fund for Distinguished Scholars from Dalian University for Dr. Shuangping Liu, National Nature Science Foundation of China [31560312, 811672781, 81973356, 81902826]
  2. Program from the Science and Technology Department of Guangdong Province of China [2017A030313890]
  3. Science and Technology Program of Guangzhou [201807010003]
  4. Program of Introducing Talents of Discipline to Universities (111 Project) [B16021]
  5. Startup Fund for Distinguished Scholars from Nankai University [63206054, 91923101]
  6. National Key R&D Program of China [2018YFC2002000]

向作者/读者索取更多资源

Energy metabolism programming, specifically the Warburg effect, plays a crucial role in cancer progression. This study demonstrates that Valproic acid (VPA) can attenuate the Warburg effect in breast cancer cells by decreasing PKM2 expression, leading to inhibited cell proliferation and colony formation. The mechanism behind this involves the inactivation of ERK1/2 phosphorylation through reduced HDAC1 expression, ultimately suppressing breast cancer growth.
Energy metabolism programming is a hallmark of cancer, and serves as a potent target of cancer therapy. Valproic acid (VPA), a broad Class I histone deacetylases (HDACs) inhibitor, has been used as a therapeutic agent for cancer. However, the detail mechanism about the potential role of VPA on the Warburg effect in breast cancer remains unclear. In this study, we highlight that VPA significantly attenuates the Warburg effect by decreasing the expression of pyruvate kinase M2 isoform (PKM2), leading to inhibited cell proliferation and reduced colony formation in breast cancer MCF-7 and MDA-MB-231 cells. Mechanistically, Warburg effect suppression triggered by VPA was mediated by inactivation of ERK1/2 phosphorylation through reduced HDAC1 expression, resulting in suppressing breast cancer growth. In summary, we uncover a novel mechanism of VPA in regulating the Warburg effect which is essential for developing the effective approach in breast cancer therapy.

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