Jinhua Dai1, Tao Wang2, Weihua Wang3, Songhua Zhang4, Yufeng Liao1, Jie Chen3. 1. Department of Clinical Laboratory, Ningbo No.2 Hospital Ningbo 315010, Zhejiang, P.R. China. 2. Department of Clinical Laboratory, The First Affiliated Hospital of Xiamen University, Fujian Medical University Xiamen 361003, Fujian, P.R. China. 3. Department of Clinical Laboratory, The Affiliated Hospital of Ningbo University Ningbo 315020, Zhejiang, P.R. China. 4. Department of Gynaecology, Ningbo No.2 Hospital Ningbo 315010, Zhejiang, P.R. China.
Abstract
AIM: To investigate the effect of mitogen-activated protein kinase 7 (MAPK7) in ovarian cancer metastasis and to explore its potential mechanism. METHODS: pcDNA-MAPK7 and siRNA-MAPK7 vectors were transfected into the human ovarian cell line OVCAR-3 based on gene silencing and overexpression methods. Effects of MAPK7 overexpression and silencing on OVCAR-3 cells proliferation, cell invasion, and migration were analyzed using the MTT (3-[4, 5-dimethylthiazol-2-yl]-2, 5-diphenyl tetrazolium bromide) assay, Matrigel methods, and Markered methods respectively. In addition, effect of MAPK7 expression on extracellular matrix (ECM) associated protein was detected using Western blot. RESULTS: Compared with the controls, MAPK7 was up-regulated when cells were transfected with pcDNA-MAPK7 plasma, as well as MAPK7 was sliced when cells were transfected with siRNA-MAPK7 plasma (P<0.05). Besides, biological function analysis performed that overexpression of MAPK7 significantly increased OVCAR-3 cell proliferation, invasion, and migration (P<0.05), while these effects were inhibited by MAPK7 silencing (P<0.05). Additionally, MAPK7 overexpression increased type II collagen expression (P<0.05). However, there was no significant difference between MAPK7 expression and type I collagen expression (P>0.05). CONCLUSION: Our data implied the up-regulated MAPK7 might contribute to ovarian cancer metastasis through up-regulating type II collagen expression and then were involved in cell biological processes such as cell proliferation, invasion, and migration. MAPK7 may be a potential therapeutic target in the clinical treatment for ovarian cancer.
AIM: To investigate the effect of mitogen-activated protein kinase 7 (MAPK7) in ovarian cancer metastasis and to explore its potential mechanism. METHODS: pcDNA-MAPK7 and siRNA-MAPK7 vectors were transfected into the human ovarian cell line OVCAR-3 based on gene silencing and overexpression methods. Effects of MAPK7 overexpression and silencing on OVCAR-3 cells proliferation, cell invasion, and migration were analyzed using the MTT (3-[4, 5-dimethylthiazol-2-yl]-2, 5-diphenyl tetrazolium bromide) assay, Matrigel methods, and Markered methods respectively. In addition, effect of MAPK7 expression on extracellular matrix (ECM) associated protein was detected using Western blot. RESULTS: Compared with the controls, MAPK7 was up-regulated when cells were transfected with pcDNA-MAPK7 plasma, as well as MAPK7 was sliced when cells were transfected with siRNA-MAPK7 plasma (P<0.05). Besides, biological function analysis performed that overexpression of MAPK7 significantly increased OVCAR-3 cell proliferation, invasion, and migration (P<0.05), while these effects were inhibited by MAPK7 silencing (P<0.05). Additionally, MAPK7 overexpression increased type II collagen expression (P<0.05). However, there was no significant difference between MAPK7 expression and type I collagen expression (P>0.05). CONCLUSION: Our data implied the up-regulated MAPK7 might contribute to ovarian cancer metastasis through up-regulating type II collagen expression and then were involved in cell biological processes such as cell proliferation, invasion, and migration. MAPK7 may be a potential therapeutic target in the clinical treatment for ovarian cancer.
Authors: J Xu; D Rodriguez; E Petitclerc; J J Kim; M Hangai; Y S Moon; G E Davis; P C Brooks; S M Yuen Journal: J Cell Biol Date: 2001-09-03 Impact factor: 10.539