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Inhibition of proliferation,migration,and invasiveness of bladder cancer cells through SAPCD2 knockdown

作     者:CHONG SHEN JIAJUN YAN YU REN ZHIRONG ZHU XIAOLONG ZHANG SHUIXIANG TAO 

作者机构:Department of UrologyShaoxing People’s HospitalShaoxing HospitalZhejiang University School of MedicineShaoxingChina 

出 版 物:《BIOCELL》 (生物细胞(英文))

年 卷 期:2024年第48卷第1期

页      面:97-109页

核心收录:

学科分类:0710[理学-生物学] 1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学] 

基  金:supported by the Medical and Health Science and Technology Program of Zhejiang Province(No.2021KY367) 

主  题:Bladder cancer SAPCD2 β-catenin c-Myc CDK4 Lithium chloride 

摘      要:Introduction:Bladder cancer(BC)has a high incidence and mortality rate *** anaphasepromoting complex domain containing 2(SAPCDC2)is over-expressed in a variety of ***:This study investigated the effects of SAPCD2 knockdown on BC ***:T24 and UMUC3 cell models and the xenografted BC tumor model with SAPCD2 knockdown were established to observe the malignant phenotype of BC cells by cell counting kit-8 assay,colony formation test,wound healing,and Transwell assay,mRNA and proteins expressions were measured with quantitative real-time polymerase chain reaction,western blotting,and tissue *** chloride agonist on the Wnt/β-catenin pathway was used to clarify the molecular mechanism of SAPCD2 ***:SAPCD2 expression was significantly higher in BC cell lines than in SVHUC-1 ***2 knockdown inhibited viability and cloning,hindered the G0/G1 phase of the cell cycle in UMUC3 and T24 cells,and decreased the migration and invasiveness of BC ***2 knockdown inhibited expression levels of cyclin D1,cyclin B1,N-cadherin,vimentin,Snail,β-catenin,c-Myc,and cyclin-dependent kinase 4,while the P21 and E-cadherin were raised by SAPCD2 ***,lithium chloride reversed the effects of SAPCD2 knockdown on the expression levels of the above proteins in UMUC3 and T24 *** vivo,SAPCD2 knockdown inhibited the volume,weight,and expression of Ki-67 andβ-catenin in tumors and increased the E-cadherin ***:SAPCD2 knockdown inhibits the malignant phenotype of BC via a pathway involvingβ-catenin.

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