@Article{biocell.2023.045303,
AUTHOR = {CHONG SHEN, JIAJUN YAN, YU REN, ZHIRONG ZHU, XIAOLONG ZHANG, SHUIXIANG TAO},
TITLE = {Inhibition of proliferation, migration, and invasiveness of bladder cancer cells through SAPCD2 knockdown},
JOURNAL = {BIOCELL},
VOLUME = {48},
YEAR = {2024},
NUMBER = {1},
PAGES = {97--109},
URL = {http://www.techscience.com/biocell/v48n1/55436},
ISSN = {1667-5746},
ABSTRACT = { <b>Introduction:</b> Bladder cancer (BC) has a high incidence and mortality rate worldwide. Suppressor anaphase-promoting complex domain containing 2 (SAPCDC2) is over-expressed in a variety of tumors. <b>Objectives:</b> This study investigated the effects of SAPCD2 knockdown on BC cells. <b>Methods:</b> 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 immunohistochemistry. Lithium chloride agonist on the Wnt/β-catenin pathway was used to clarify the molecular mechanism of SAPCD2 knockdown. <b>Results:</b> SAPCD2 expression was significantly higher in BC cell lines than in SV-HUC-1 cells. SAPCD2 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 cells. SAPCD2 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 knockdown. Furthermore, lithium chloride reversed the effects of SAPCD2 knockdown on the expression levels of the above proteins in UMUC3 and T24 cells. <i>In vivo</i>, SAPCD2 knockdown inhibited the volume, weight, and expression of Ki-67 and β-catenin in tumors and increased the E-cadherin expression. <b>Conclusion:</b> SAPCD2 knockdown inhibits the malignant phenotype of BC via a pathway involving β-catenin.},
DOI = {10.32604/biocell.2023.045303}
}