Experimental and Molecular Medicine (Oct 2018)

Cyclin B1 stability is increased by interaction with BRCA1, and its overexpression suppresses the progression of BRCA1-associated mammary tumors

  • Eun Kyung Choi,
  • Jeong-A Lim,
  • Jong Kwang Kim,
  • Moon Sun Jang,
  • Sun Eui Kim,
  • Hye Jung Baek,
  • Eun Jung Park,
  • Tae Hyun Kim,
  • Chu-Xia Deng,
  • Rui-Hong Wang,
  • Sang Soo Kim

DOI
https://doi.org/10.1038/s12276-018-0169-z
Journal volume & issue
Vol. 50, no. 10
pp. 1 – 16

Abstract

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Breast cancer: A protein link for treatment? The role of disrupted activity of the protein BRCA1 in the progression of breast cancer has been clarified, suggesting that targeting another protein with which it interacts could offer a new route to treatment. Mutations of BRCA1 are known to predispose women to both breast and ovarian cancers. Researchers led by Sang Soo Kim (National Cancer Center, South Korea) and Rui-Hong Wang (University of Macau, China) studied the interaction with a protein called cyclin B1 that controls cell growth and division. They found that, in mitosis, BRCA1 interacts with and stabilizes cyclin B1, explaining why the loss of BRCA1 can disrupt the G2/M cell cycle control and accumulate the genetic instability. Treatment of Brca1-mutant mammary tumors with vinblastine, which alters cyclin B1 level, significantly reduced tumor progression with reduction of survival and induction of apoptosis.