title: RNAi-mediated knockdown of MCM7 gene on CML cells and its therapeutic potential for leukemia.
abstract: MCM7 is one of the subunits of MCM2-7 complex, which is essential to DNA replication licensing and the control of cell cycle progression. It has been demonstrated that MCM7 participates in mRNA transcription and DNA damage regulation as well. MCM7 gene is found to be over-expressed in multiple cancers, but there are few reports about its effect in leukemia. Recent studies have proven that MCM7 expression has a relationship with diagnosis and prognosis, which has led to their potential clinical application as a marker for cancer screening. RNA interference (RNAi) is a biological process in which RNA molecules inhibit gene expression, typically by causing the destruction of specific mRNA molecules. It is a valuable research tool, which is widely used in cell culture and living organisms as well as in medicine recent years. It is indicated that RNAi application for targeting functional carcinogenic molecules, tumor resistance to chemotherapy and radiotherapy is required in cancer treatment. Gene products knockdown by RNAi technology exerts anti-proliferative and pro-apoptotic effects upon cell culture systems, animal models and in clinical trials in the most studies. In the present study, we found that MCM7 highly expressed in K562 cells rather than that in normal neutrophils. Thus, lentivirus-mediated shRNA targeting MCM7 was used to suppress its endogenous expression in K562 cells and develop a novel therapeutic strategy for leukemia.
authors.affiliation: Department of Hematology and Oncology, Medical School, Zhongda Hospital, Southeast University, 87 Dingjiaqiao, Nanjing, 210009, China.
authors.forename: Liang
authors.initials: L
authors.lastname: Tian
authors.affiliation: Department of Digestive System, Medical School, Zhongda Hospital, Southeast University, Nanjing, China.
authors.forename: Juan
authors.initials: J
authors.lastname: Liu
authors.affiliation: Department of Clinical Laboratory, Medical School, Southeast University, Nanjing, China.
authors.forename: Guo-Hua
authors.initials: GH
authors.lastname: Xia
authors.affiliation: Department of Hematology and Oncology, Medical School, Zhongda Hospital, Southeast University, 87 Dingjiaqiao, Nanjing, 210009, China. health-ZJY@sohu.com.
authors.forename: Bao-An
authors.initials: BA
authors.lastname: Chen
mesh_terms: D000818:Animals; D015536:Down-Regulation; D055785:Gene Knockdown Techniques; D006801:Humans; D020014:K562 Cells; D016086:Lentivirus / Q000235:genetics; D004915:Leukemia, Erythroblastic, Acute / Q000235:genetics* / Q000378:metabolism / Q000628:therapy; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008819:Mice, Nude; D064168:Minichromosome Maintenance Complex Component 7 / Q000096:biosynthesis / Q000172:deficiency / Q000235:genetics*; D058990:Molecular Targeted Therapy; D034622:RNA Interference; D034741:RNA, Small Interfering / Q000008:administration & dosage / Q000235:genetics; D011897:Random Allocation; D023041:Xenograft Model Antitumor Assays
chemical_list: D034741:RNA, Small Interfering; C101624:MCM7 protein, human; D064168:Minichromosome Maintenance Complex Component 7
keywords: K562 cell; Lentivirus-mediated siRNA; Leukemia; MCM7 gene