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Calponin 3 promotes invasion and drug resistance of colon cancer cells

World Journal of Gastrointestinal Oncology 2019年第11期11卷 971-982页

作者： Vidhya A Nair Noura A Al-khayyal sivaramakrishnan sivaperumal Wael M Abdel-Rahman Environment and Cancer Research Group Sharjah Institute for Medical ResearchUniversity of SharjahSharjah 27272United Arab Emirates College of Medicine and Sharjah Institute for Medical Research University of SharjahSharjah 27272United Arab Emirates Department of Biotechnology Bharathidasan UniversityTiruchirappalli 620024India Department of Medical Laboratory Sciences College of Health Sciences and Environment and Cancer Research GroupSharjah Institute for Medical ResearchUniversity of SharjahSharjah 27272United Arab Emirates

BACKGROUND Calponin 3(CNN3)is an actin-binding protein expressed in smooth muscle and non-smooth muscle *** is required for cytoskeletal rearrangement and wound *** To dissect the role of CNN3 in carcinogenesis with a focus on colon *** A total of 20 cancer cell lines(8 breast,11 colon,and HeLa cervical cancer cell as a positive control for mesenchymal phenotype)and 57 formalin-fixed,paraffinembedded sections from archived sporadic colorectal carcinomas were included in this ***3 expression analysis by western blot or immunohistochemistry was followed by functional *** CNN3 gene was silenced by specific small interfering RNA(commonly known as siRNA),followed by confirmation of the silencing efficiency by western ***,the silenced cells and control siRNA-transfected cells were analyzed for changes in epithelial and mesenchymal markers,invasion,and response to 5-fluoruracil *** also performed proteomics analysis using a phospho-kinase array-based panel of 45 *** CNN3 showed positive expression in 6/8 breast and 9/11 colon cancer lines and in HeLa ***,the colorectal adenocarcinoma line SW480 was negative,while the cell line developed from its matching lymph node metastasis(SW620)was positive for ***3 expression was fairly consistent with the metastatic phenotype in colon cancer because it was absent in one other colon cell line from a primary site and expressed in all *** selected SW620 for subsequent functional ***3-silenced SW620 cells showed a reduction in collagen invasion and loss of mesenchymal ***3 silencing caused an increase in the SW620 colon cancer cell sensitivity to *** array-based proteomics analysis showed that CNN3 silencing in SW620 reduced extracellular signal-regulated kinase,β-Catenin,mutant p53,c-Jun,and heat shock protein 60 activities but increased that of checkpoint kinase ***3 was expressed in 20/57(35%)co

关键词： β-Catenin Calponin 3 Colon cancer Epithelial-mesenchymal transition Invasion Metastasis

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