Cathepsin B Is Upregulated and Mediates ECM Degradation in Colon Adenocarcinoma HT29 Cells Overexpressing Snail

Cells
Jakub KryczkaJoanna Boncela

Abstract

During tumor development and ongoing metastasis the acquisition of mesenchymal cell traits by epithelial carcinoma cells is achieved through a programmed phenotypic shift called the epithelial-to-mesenchymal transition, EMT. EMT contributes to increased cancer cell motility and invasiveness mainly through invadosomes, the adhesion structures that accompany the mesenchymal migration. The invadosomes and their associated proteases restrict protease activity to areas of the cell in direct contact with the ECM, thus precisely controlling cell invasion. Our data prove that Snail-overexpressing HT-29 cells that imitate the phenotype of colon cancer cells in the early stage of the EMT showed an increase in the expression and pericellular activity of cathepsin B. It appears that the pericellular localization of cathepsin B, also observed in colon and rectum adenocarcinoma tissue samples, plays a key role in its function.

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Citations

Sep 5, 2019·Cancer Metastasis Reviews·Julia MitschkeThomas Reinheckel
May 10, 2019·Cancer Metastasis Reviews·Kyungmin JiBonnie F Sloane
Sep 13, 2020·Cell Biochemistry and Biophysics·Chun-Hua WangFu-Ming Tsai
Dec 1, 2020·Bioorganic & Medicinal Chemistry·Lorenzo CianniAnwar Shamim
Dec 3, 2020·Cancers·Jakub KryczkaJoanna Boncela
Feb 3, 2021·Journal of Microbiology and Biotechnology·Chijian ZhangTinggang He
Jun 17, 2021·Cellular and Molecular Life Sciences : CMLS·Abudureyimu TuerhongChen Liang
Mar 13, 2020·Bioconjugate Chemistry·In-Cheol SunKwangmeyung Kim

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Methods Mentioned

BETA
GTPase
xenograft
Profiler
Protease Array
confocal microscopy
zymography

Software Mentioned

EZ
C1
Human Protein Atlas

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