Fei Cao1, Li-Xue Yin2. 1. School of Medicine, University of Electronic Science and Technology of China, Chengdu 610054, China. 2. School of Medicine, University of Electronic Science and Technology of China, Chengdu 610054, China; Key Laboratory of Ultrasound in Cardiac Electrophysiology and Biomechanics of Sichuan Province, Department of Cardiovascular Ultrasound and Non-Invasive Cardiology, Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital, Chengdu 610072, China. Electronic address: yinlixue_cardiac@163.com.
Abstract
BACKGROUND: Hepatocellular carcinoma (HCC) is a primary cause of cancer mortality. PAK1 plays key roles in many types of cancers. However, the role of PAK1 in HCC is not clear. METHODS: qRT-PCR and Western blotting were used to determine expressions of PAK1, Snail and epithelial mesenchymal transition (EMT)-related proteins. Luciferase reporter assay was used to measure the interaction between PAK1 and Snail. Wound healing, transwell, colony formation assays and flow cytometry were used to assess cell migration, invasion, proliferation and apoptosis. Mouse tumor xenograft model was used to determine the effect of PAK1 on tumor growth in vivo. RESULTS: PAK1 and Snail were up-regulated in HCC cells. PAK1 knockdown suppressed cell proliferation, migration and invasion, and increased apoptosis of HCC cells. PAK1 knockdown also inhibited tumor growth in vivo. Mechanistically, PAK1 promoted EMT by targeting Snail. Knockdown of PAK1 could up-regulate pro-apoptotic proteins but down-regulate proliferation-related proteins via suppressing β-catenin signaling pathway. CONCLUSION: PAK1 promotes EMT process by increasing Snail, and facilitates progression of HCC by activating β-catenin pathway.
BACKGROUND:Hepatocellular carcinoma (HCC) is a primary cause of cancer mortality. PAK1 plays key roles in many types of cancers. However, the role of PAK1 in HCC is not clear. METHODS: qRT-PCR and Western blotting were used to determine expressions of PAK1, Snail and epithelial mesenchymal transition (EMT)-related proteins. Luciferase reporter assay was used to measure the interaction between PAK1 and Snail. Wound healing, transwell, colony formation assays and flow cytometry were used to assess cell migration, invasion, proliferation and apoptosis. Mousetumor xenograft model was used to determine the effect of PAK1 on tumor growth in vivo. RESULTS:PAK1 and Snail were up-regulated in HCC cells. PAK1 knockdown suppressed cell proliferation, migration and invasion, and increased apoptosis of HCC cells. PAK1 knockdown also inhibited tumor growth in vivo. Mechanistically, PAK1 promoted EMT by targeting Snail. Knockdown of PAK1 could up-regulate pro-apoptotic proteins but down-regulate proliferation-related proteins via suppressing β-catenin signaling pathway. CONCLUSION:PAK1 promotes EMT process by increasing Snail, and facilitates progression of HCC by activating β-catenin pathway.
Authors: Marc Micó-Carnero; Araní Casillas-Ramírez; Alfredo Sánchez-González; Carlos Rojano-Alfonso; Carmen Peralta Journal: Biomedicines Date: 2022-04-23
Authors: Gang Chen; Jiangtao Liao; Yan Xu; Yinyun Chen; Juan Li; Guangkui Bu; Qingqing Li Journal: Cancer Manag Res Date: 2022-05-13 Impact factor: 3.602