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Cathepsin B: A sellsword of cancer progression

Thumbnail
2019
10.1016@j.canlet.2019.02.035.pdf (1.351Mb)
Аутори
Mijanović, Olja
Branković, Ana
Panin, Alexander N.
Savchuk, Solomiia
Timashev, Peter
Ulasov, llya
Lesniak, Maciej S.
Информативни прилог (Рецензирана верзија)
Метаподаци
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Апстракт
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 nex...t – 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.

Кључне речи:
autophagy / cathepsin B / migration / tumor
Извор:
Cancer Letters, 2019, 449, 207-214
Издавач:
  • Elsevier
Напомена:
  • This is the peer-reviewed version of the article: Mijanović, Olja, Ana Branković, Alexander N. Panin, Solomiia Savchuk, Peter Timashev, Ilya Ulasov, and Maciej S. Lesniak. 2019. ‘Cathepsin B: A Sellsword of Cancer Progression’. Cancer Letters 449 (May): 207–14. https://doi.org/10.1016/j.canlet.2019.02.035.

DOI: 10.1016/j.canlet.2019.02.035

ISSN: 0304-3835

WoS: 000463130200021

Scopus: 2-s2.0-85062032514
[ Google Scholar ]
13
8
URI
http://jakov.kpu.edu.rs/handle/123456789/891
Колекције
  • Radovi istraživača / Researchers' publications
Институција
Jakov
TY  - JOUR
AU  - Mijanović, Olja
AU  - Branković, Ana
AU  - Panin,  Alexander N.
AU  - Savchuk, Solomiia
AU  - Timashev, Peter
AU  - Ulasov, llya
AU  - Lesniak, Maciej S.
PY  - 2019
UR  - http://jakov.kpu.edu.rs/handle/123456789/891
AB  - 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.
PB  - Elsevier
T2  - Cancer Letters
T1  - Cathepsin B: A sellsword of cancer progression
VL  - 449
SP  - 207
EP  - 214
DO  - 10.1016/j.canlet.2019.02.035
ER  - 
@article{
author = "Mijanović, Olja and Branković, Ana and Panin,  Alexander N. and Savchuk, Solomiia and Timashev, Peter and Ulasov, llya and Lesniak, Maciej S.",
year = "2019",
url = "http://jakov.kpu.edu.rs/handle/123456789/891",
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.",
publisher = "Elsevier",
journal = "Cancer Letters",
title = "Cathepsin B: A sellsword of cancer progression",
volume = "449",
pages = "207-214",
doi = "10.1016/j.canlet.2019.02.035"
}
Mijanović O, Branković A, Panin AN, Savchuk S, Timashev P, Ulasov L, Lesniak MS. Cathepsin B: A sellsword of cancer progression. Cancer Letters. 2019;449:207-214
Mijanović, O., Branković, A., Panin, A. N., Savchuk, S., Timashev, P., Ulasov, l.,& Lesniak, M. S. (2019). Cathepsin B: A sellsword of cancer progression.
Cancer LettersElsevier., 449, 207-214.
https://doi.org/10.1016/j.canlet.2019.02.035
Mijanović Olja, Branković Ana, Panin  Alexander N., Savchuk Solomiia, Timashev Peter, Ulasov llya, Lesniak Maciej S., "Cathepsin B: A sellsword of cancer progression" 449 (2019):207-214,
https://doi.org/10.1016/j.canlet.2019.02.035 .

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