Cathepsin B: A sellsword of cancer progression

Olja Mijanović, Ana Branković, Alexander N. Panin, Solomiia Savchuk, Peter Timashev, Ilya Ulasov, Maciej S. Lesniak*

*Corresponding author for this work

Research output: Contribution to journalShort survey

1 Scopus citations

Abstract

Clinical, biochemical and molecular biology studies have identified lysosome-encapsulated cellular proteases as critical risk factors for cancer progression. Cathepsins represent a group of such proteases aimed at maintenance of cellular homeostasis. Nevertheless, recent reports suggest that Cathepsin B executes other cellular programs such as controlling tumor growth, migration, invasion, angiogenesis, and metastases development. In fact, elevated levels of Cathepsins are found under different pathological conditions including inflammation, infection, neurodegenerative disease, and cancer. Furthermore, the discovery of Cathepsin B secretion and function as an extracellular matrix protein has broadened our appreciation for the impact of Cathepsin B on cancer progression. Underneath a façade of an intracellular protease with limited therapeutic potential hides a central role of cathepsins in extracellular functions. Moreover, this role is incredibly diverse from one condition to the next – from driving caspase-dependent apoptosis to facilitating tumor neovascularization and metastasis. Here we discuss the role of Cathepsin B in the oncogenic process and perspective the use of Cathepsin B for diagnostic and therapeutic applications.

Original languageEnglish (US)
Pages (from-to)207-214
Number of pages8
JournalCancer Letters
Volume449
DOIs
Publication statusPublished - May 1 2019

    Fingerprint

Keywords

  • Autophagy
  • Cathepsin B
  • Migration
  • Tumor

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

Cite this

Mijanović, O., Branković, A., Panin, A. N., Savchuk, S., Timashev, P., Ulasov, I., & Lesniak, M. S. (2019). Cathepsin B: A sellsword of cancer progression. Cancer Letters, 449, 207-214. https://doi.org/10.1016/j.canlet.2019.02.035