CTSC promotes tumorigenesis in bladder cancer by activating Wnt/β-Catenin signaling

Author:

Wang Xinsheng1,Jia Yong2,Wang Dawen2

Affiliation:

1. Tianjin Medical University

2. Qingdao Municipal Hospital

Abstract

Abstract

Cathepsin C (CTSC) participates in the development of numerous cancers. The function of bladder cancer (BCa) is still largely unknown. Bioinformatics prediction, RT-qPCR assay, and Western blotting assay determined the level of expression of CTSC in BCa tissues, para-cancer tissues, BCa cells, and normal uroepithelial cells (SV-HUC-1). Colony formation assay, CCK-8 assay, and Transwell assay were utilized to ascertain the involvement of CTSC in BCa. In addition, the effect of CTSC on BCa was further studied by animal experiments in vivo. The findings affirmed that CTSC exhibited a heightened expression level in BCa cells and tissues, and the overexpression of CTSC substantially enhanced the activity, proliferation, migration, and invasion of BCa cells, while suppression of CTSC repressed the above biological phenotypes. CTSC could both activate the Wnt/β-Catenin signaling pathway and up-regulate DIAPH3 expression. Overexpression of CTSC combined with knockdown of DIAPH3 could partially reverse the impact of CTSC on the biological behavior of BCa cells and the Wnt/β-Catenin signaling pathway activation. CTSC could up-regulate DIAPH3 and activate the aforementioned pathway to enhance the activity, proliferation, migration, and invasion of cells from BCa.

Publisher

Research Square Platform LLC

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