Targeting CD44 and other pleiotropic co-receptors as a means for broad inhibition of tumor growth and metastasis

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Název: Targeting CD44 and other pleiotropic co-receptors as a means for broad inhibition of tumor growth and metastasis
Autoři: Lisa-Marie Mehner, Leonel Munoz-Sagredo, Steffen Joachim Sonnentag, Sven Máté Treffert, Véronique Orian-Rousseau
Zdroj: Clin Exp Metastasis
Clinical and Experimental Metastasis
Informace o vydavateli: Springer Science and Business Media LLC, 2024.
Rok vydání: 2024
Témata: 0301 basic medicine, ddc:610, 0303 health sciences, Antineoplastic Agents, Review, Medicine & health, 3. Good health, 03 medical and health sciences, Hyaluronan Receptors, Neoplasms, Humans, Animals, Molecular Targeted Therapy, Neoplasm Metastasis, Cancer, Pleiotropicity, Humans [MeSH], Metastasis, Neoplasm Metastasis [MeSH], Hyaluronan Receptors/metabolism [MeSH], Antineoplastic Agents/pharmacology [MeSH], Animals [MeSH], Neoplasms/metabolism [MeSH], Neoplasms/pathology [MeSH], CD44, Antineoplastic Agents/therapeutic use [MeSH], Co-receptors, Signal Transduction [MeSH], Molecular Targeted Therapy/methods [MeSH], Signal Transduction
Popis: Although progress has been made in the treatment of cancer, particularly for the four major types of cancers affecting the lungs, colon, breast and prostate, resistance to cancer treatment often emerges upon inhibition of major signaling pathways, which leads to the activation of additional pathways as a last-resort survival mechanism by the cancer cells. This signaling plasticity provides cancer cells with a level of operational freedom, reducing treatment efficacy. Plasticity is a characteristic of cancer cells that are not only able to switch signaling pathways but also from one cellular state (differentiated cells to stem cells or vice versa) to another. It seems implausible that the inhibition of one or a few signaling pathways of heterogeneous and plastic tumors can sustain a durable effect. We propose that inhibiting molecules with pleiotropic functions such as cell surface co-receptors can be a key to preventing therapy escape instead of targeting bona fide receptors. Therefore, we ask the question whether co-receptors often considered as “accessory molecules” are an overlooked key to control cancer cell behavior.
Druh dokumentu: Article
Other literature type
Popis souboru: application/pdf
Jazyk: English
ISSN: 1573-7276
0262-0898
DOI: 10.1007/s10585-024-10292-4
DOI: 10.5445/ir/1000171434
Přístupová URL adresa: https://pubmed.ncbi.nlm.nih.gov/38761292
https://publikationen.bibliothek.kit.edu/1000171434
https://publikationen.bibliothek.kit.edu/1000171434/153027455
https://doi.org/10.5445/IR/1000171434
https://repository.publisso.de/resource/frl:6524666
Rights: CC BY
Přístupové číslo: edsair.doi.dedup.....cea998c31629d49084678cda9db86d91
Databáze: OpenAIRE
Popis
Abstrakt:Although progress has been made in the treatment of cancer, particularly for the four major types of cancers affecting the lungs, colon, breast and prostate, resistance to cancer treatment often emerges upon inhibition of major signaling pathways, which leads to the activation of additional pathways as a last-resort survival mechanism by the cancer cells. This signaling plasticity provides cancer cells with a level of operational freedom, reducing treatment efficacy. Plasticity is a characteristic of cancer cells that are not only able to switch signaling pathways but also from one cellular state (differentiated cells to stem cells or vice versa) to another. It seems implausible that the inhibition of one or a few signaling pathways of heterogeneous and plastic tumors can sustain a durable effect. We propose that inhibiting molecules with pleiotropic functions such as cell surface co-receptors can be a key to preventing therapy escape instead of targeting bona fide receptors. Therefore, we ask the question whether co-receptors often considered as “accessory molecules” are an overlooked key to control cancer cell behavior.
ISSN:15737276
02620898
DOI:10.1007/s10585-024-10292-4