title: JARID1B modulates lung cancer cell proliferation and invasion by regulating p53 expression.
abstract: Although three therapeutic modalities (surgical resection, chemotherapy, and radiotherapy) have been established, long-term survival for lung cancer patients is still generally poor. Until now, the mechanisms of lung cancer genesis remain elusive. The JARID1B is a histone demethylase that has been proposed as oncogene in several types of human cancer, but its clinical significance and functional role in human non-small cell lung cancer (NSCLC) remain unclear. In present study, we found that JARID1B was overexpressed in lung cancer cell lines and lung cancer tissues but not in normal lung tissues. The proliferation and invasive potential of lung cancer cells was significantly increased by ectopic expression of JARID1B. Contrarily, RNA interference targeting JARID1B in lung cancer cells significantly decreased the proliferation and invasive potential of cells. Moreover, we also found that the expression of p53 was modulated by JARID1B. Overexpressed JARID1B cell exhibited greatly decreased p53 expression, whereas silencing of JARID1B expression dramatically increased p53 expression at both the messenger RNA (mRNA) and protein levels. Inhibition of p53 by small interfering RNA (siRNA) reversed the shJARID1B-induced suppression of proliferation and invasion. Our results collectively suggested that JARID1B expressed in lung cancer played a role in lung cancer cells proliferation and invasion, which may be partly associated with the p53 expression.
authors: Department of Oncology, The Second Affiliated Hospital of Soochow University, Suzhou, China.
authors: Xudong
authors: X
authors: Shen
authors: Department of Oncology, The Second Affiliated Hospital of Soochow University, Suzhou, China.
authors: Zhixiang
authors: Z
authors: Zhuang
authors: Department of Oncology, The Second Affiliated Hospital of Soochow University, Suzhou, China.
authors: Yusong
authors: Y
authors: Zhang
authors: Department of Oncology, The Second Affiliated Hospital of Soochow University, Suzhou, China.
authors: Zhigang
authors: Z
authors: Chen
authors: Department of Oncology, The Second Affiliated Hospital of Soochow University, Suzhou, China.
authors: Liqin
authors: L
authors: Shen
authors: Department of Oncology, The Second Affiliated Hospital of Soochow University, Suzhou, China.
authors: Wangyang
authors: W
authors: Pu
authors: Department of Oncology, The Second Affiliated Hospital of Soochow University, Suzhou, China.
authors: Lei
authors: L
authors: Chen
authors: Department of Thoracic Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, China. zhonghuaxutg@sina.cn.
authors: Zhonghua
authors: Z
authors: Xu
mesh_terms: D000818:Animals; D063646:Carcinogenesis / Q000235:genetics; D002289:Carcinoma, Non-Small-Cell Lung / Q000235:genetics* / Q000473:pathology; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000235:genetics*; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D056484:Jumonji Domain-Containing Histone Demethylases / Q000037:antagonists & inhibitors / Q000096:biosynthesis* / Q000235:genetics; D051379:Mice; D009361:Neoplasm Invasiveness / Q000235:genetics; D009687:Nuclear Proteins / Q000037:antagonists & inhibitors / Q000096:biosynthesis* / Q000235:genetics; D034622:RNA Interference; D012097:Repressor Proteins / Q000037:antagonists & inhibitors / Q000096:biosynthesis* / Q000235:genetics; D016159:Tumor Suppressor Protein p53 / Q000096:biosynthesis* / Q000235:genetics; D023041:Xenograft Model Antitumor Assays
chemical_list: D009687:Nuclear Proteins; D012097:Repressor Proteins; C495901:TP53 protein, human; D016159:Tumor Suppressor Protein p53; D056484:Jumonji Domain-Containing Histone Demethylases; C119611:KDM5B protein, human
keywords: Invasion; JARID1B; Lung cancer; Proliferation; p53