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Beta-elemene inhibits breast cancer metastasis through blocking pyruvate kinase M2 dimerization and nuclear

Yanhong Pan1, Wei Wang1, Shuai Huang1

  • 1Jiangsu Key Laboratory for Pharmacology and Safety Evaluation of Chinese Materia Medica, School of Pharmacy, Nanjing University of Chinese Medicine, Nanjing, China.

Journal of Cellular and Molecular Medicine
|July 26, 2019
PubMed

Insights

Beta-elemene inhibits breast cancer metastasis by targeting pyruvate kinase M2 (PKM2). This natural compound blocks PKM2

Area of Science:

  • Oncology
  • Biochemistry
  • Molecular Biology

Background:

  • Pyruvate kinase M2 (PKM2) regulates aerobic glycolysis and is a cancer therapy target.
  • The role of PKM2 in cancer metastasis is not well understood.

Purpose of the Study:

  • To investigate the relationship between PKM2 and breast cancer metastasis.
  • To explore the anti-metastatic effects of beta-elemene (β-elemene) and its mechanism involving PKM2.

Main Methods:

  • Studied the effect of β-elemene on breast cancer cell migration and invasion in vitro and metastasis in vivo.
  • Assessed β-elemene's impact on aerobic glycolysis, glucose utilization, and pyruvate/lactate production.
  • Analyzed PKM2's dimeric/tetrameric transformation, nuclear translocation, and downstream targets (EGFR, GLUT1, LDHA).
  • Investigated the role of importin α5 and reversal effects of fructose-1,6-bisphosphate (FBP) and L-cysteine.

Main Results:

  • β-elemene significantly inhibited breast cancer cell migration, invasion, and in vivo metastasis.
  • β-elemene suppressed aerobic glycolysis by inhibiting PKM2 activity, decreasing glucose use, pyruvate, and lactate production.
  • β-elemene blocked PKM2 nuclear translocation and reduced EGFR, GLUT1, and LDHA expression, partly via importin α5.
  • FBP and L-cysteine partially reversed β-elemene's effects on migration, invasion, and PKM2.

Conclusions:

  • Tetrameric PKM2 and its nuclear translocation are crucial for cancer metastasis.
  • β-elemene acts as a promising anti-metastatic agent by inhibiting aerobic glycolysis through modulation of PKM2 dimeric transformation and nuclear translocation.
Keywords:
aerobic glycolysisbeta-elemenebreast cancermetastasispyruvate kinase M2

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