Laboratory Medicine ›› 2018, Vol. 33 ›› Issue (7): 657-662.DOI: 10.3969/j.issn.1673-8640.2018.07.019

• Orginal Article • Previous Articles     Next Articles

Targeting inhibition on the overexpressed HRR proteins in cancer cells to enhance chemoradio-sensitivity

ZHU Jiabei1, HUANG Nan2, CUI Zhongqi2, YANG Qingyuan2, PAN Qiuhui1   

  1. 1. Department of Clinical Laboratory,Shanghai Children's Medical Center,Shanghai Jiaotong University School of Medicine,Shanghai 200127,China
    2. Department of Clinical Laboratory,Shanghai Tenth People's Hospital,Tongji University,Shanghai 200072,China
  • Received:2017-05-15 Online:2018-07-30 Published:2018-07-27

Abstract:

Homologous recombination repair (HRR) is a prominent approach for repairing exogenous and endogenous DNA double-stranded breaks in mammalian cells,which can preserve genome integrity and stability to ensure the function and viability of mammalian cells. It has been widely recognized as a tumor suppressor. Recent studies have found that cancer cells with increased expression of HRR proteins hold powerful repair vitality,causing resistance to chemotherapies and radiotherapies by repairing DNA damage triggered by these curing methods,impeding cell apoptosis pathway and activating cell survival pathway,thus greatly promoting cancer cell survival. These overexpressed proteins play an oncogenic role in cancer cells,as indicate by maintaining genome stability of these cells and promoting tumorigenesis and tumor development,thereby providing potential targets of precision cancer therapy. Targeting inhibition through drugs on the overexpressed HRR proteins in cancer cells will not only stimulate cell apoptosis,but also remarkably enhance the cellular sensitivity to ionizing radiation and cytotoxic chemotherapies.

Key words: Homologous recombination repair protein, Oncogene, Tumor therapy

CLC Number: