Crk and CrkL as Therapeutic Targets for Cancer Treatment.
Crk
CrkL
cancer
cell proliferation
epithelial-mesenchymal transition
invasion
migration
transformation
Journal
Cells
ISSN: 2073-4409
Titre abrégé: Cells
Pays: Switzerland
ID NLM: 101600052
Informations de publication
Date de publication:
27 03 2021
27 03 2021
Historique:
received:
01
03
2021
revised:
20
03
2021
accepted:
24
03
2021
entrez:
3
4
2021
pubmed:
4
4
2021
medline:
21
10
2021
Statut:
epublish
Résumé
Crk and CrkL are cellular counterparts of the viral oncoprotein v-Crk. Crk and CrkL are overexpressed in many types of human cancer, correlating with poor prognosis. Furthermore, gene knockdown and knockout of Crk and CrkL in tumor cell lines suppress tumor cell functions, including cell proliferation, transformation, migration, invasion, epithelial-mesenchymal transition, resistance to chemotherapy drugs, and in vivo tumor growth and metastasis. Conversely, overexpression of tumor cells with Crk or CrkL enhances tumor cell functions. Therefore, Crk and CrkL have been proposed as therapeutic targets for cancer treatment. However, it is unclear whether Crk and CrkL make distinct or overlapping contributions to tumor cell functions in various cancer types because Crk or CrkL have been examined independently in most studies. Two recent studies using colorectal cancer and glioblastoma cells clearly demonstrated that Crk and CrkL need to be ablated individually and combined to understand distinct and overlapping roles of the two proteins in cancer. A comprehensive understanding of individual and overlapping roles of Crk and CrkL in tumor cell functions is necessary to develop effective therapeutic strategies. This review systematically discusses crucial functions of Crk and CrkL in tumor cell functions and provides new perspectives on targeting Crk and CrkL in cancer therapy.
Identifiants
pubmed: 33801580
pii: cells10040739
doi: 10.3390/cells10040739
pmc: PMC8065463
pii:
doi:
Substances chimiques
Adaptor Proteins, Signal Transducing
0
CRKL protein
0
Proto-Oncogene Proteins c-crk
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Katharine B. Richardson grant
ID : 2019 Summer
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