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Rac1 repression reverses chemoresistance by targeting tumor metabolism.

Authors
  • Ganapathy-Kanniappan, Shanmugasundaram1
  • 1 Russell H. Morgan Department of Radiology and Radiological Science, Division of Interventional Radiology, The Johns Hopkins University School of Medicine , Baltimore, MD, USA.
Type
Published Article
Journal
Cancer Biology & Therapy
Publisher
Landes Bioscience
Publication Date
Oct 02, 2020
Volume
21
Issue
10
Pages
888–890
Identifiers
DOI: 10.1080/15384047.2020.1809923
PMID: 32866423
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Tumor metabolism is exemplified by the increased rate of glucose utilization, a biochemical signature of cancer cells. The enhanced glucose hydrolysis enabled by the augmentation of glycolytic flux and the pentose phosphate pathway (PPP) plays a pivotal role in the growth and survival of neoplastic cells. In a recent report, it has been shown that in human breast cancer the GTP binding protein, Rac1 enables resistance to therapy, particularly against the DNA-damaging therapeutics. Significantly, the findings demonstrate that Rac1-dependent chemoresistance involves the upregulation of glycolytic flux as well as PPP. Using multiple approaches, the study demonstrates that disruption of Rac1 activity sensitizes cancer cells to DNA-damaging agents. More importantly, the data uncover a previously unknown PPP regulatory role of Rac1 in breast cancer. Finally, the authors also show the effectiveness and the feasibility of in vivo targeting of Rac1 to enhance the chemosensitivity of breast cancer. This elegant report provokes scientific curiosity to expand our understanding of the intricacies of the role and regulation of Rac1 in cancer.

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