KangSheng- Liu,Weimin-Fang,Er Hu-Sun,Yajun Chen. Roles of endoplasmic reticulum stress and apoptosis signaling pathways in gynecologic tumor cells: A systematic review. Oncol Transl Med, 2017, 3: 131-135.
Roles of endoplasmic reticulum stress and apoptosis signaling pathways in gynecologic tumor cells: A systematic review
Received:October 23, 2016  Revised:March 24, 2017
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KeyWord:endoplasmic reticulum (ER); unfolded protein response (UPR); inositol-requiring-JNK (IRE1-JNK); caspase; CCAAT-enhancer-binding protein homologous protein (CHOP); gynecologic tumor cell
Author NameAffiliationDepartment
KangSheng- Liu Department of Clinical Laboratory, Nanjing Obstetrics and Gynecology Hospital Affiliated to Nanjing Medical University, Nanjing 210029, China 医学诊断实验科
Weimin-Fang Department of Clinical Laboratory, Nanjing Obstetrics and Gynecology Hospital Affiliated to Nanjing Medical University, Nanjing 210029, China 医学诊断实验科
Er Hu-Sun Department of Obstetrics and Gynecology, Nanjing Obstetrics and Gynecology Hospital Affiliated to Nanjing Medical University, Nanjing 210029, China Department of Obstetrics and Gynecology
Yajun Chen Department of Clinical Laboratory, Nanjing Obstetrics and Gynecology Hospital Affiliated to Nanjing Medical University, Nanjing 210029, China Department of Clinical Laboratory
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Abstract:
      Efficient functioning of the endoplasmic reticulum (ER) is very important for most cellular activities, such as protein folding and modification. The ER closely interacts with other organelles, including the Golgi body, endosome, membrane, and mitochondria, providing lipids and proteins for the repair of these organelles. ER stress can be induced by various abnormal materials in the cell. ER stress is a compensatory intracellular environment disorder that occurs during areaction. ER can sense the stress and respond to it through translational attenuation, upregulation of the genes for ER chaperones and related proteins, and degradation of unfolded proteins by a quality-control system, but excessive ER activation can cause cell death. The Pubmed and Web of Science databases were searched for full-text articles, and the terms “endoplasmic reticulum stress / unfolded protein response / gynecologic tumor cell apoptosis” were used as key words. Thirty-five studies of ER stress and unfolded protein response published from 2000 to 2016 were analyzed. Stress triggers apoptosis through a variety of signaling pathways. Increasing evidence has shown that the ER plays an important role in tumor cell diseases. The present review discusses the molecular mechanisms underlying unfolded protein response and its ability to promote survival and proliferation in gynecologic tumor cells.
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