PMID- 19787002
OWN - NLM
STAT- MEDLINE
DCOM- 20091214
LR  - 20211020
IS  - 1759-4782 (Electronic)
IS  - 1759-4774 (Linking)
VI  - 6
IP  - 10
DP  - 2009 Oct
TI  - Src kinases as therapeutic targets for cancer.
PG  - 587-95
LID - 10.1038/nrclinonc.2009.129 [doi]
AB  - Src family kinases (SFKs) have a critical role in cell adhesion, invasion, 
      proliferation, survival, and angiogenesis during tumor development. SFKs comprise 
      nine family members that share similar structure and function. Overexpression or 
      high activation of SFKs occurs frequently in tumor tissues and they are central 
      mediators in multiple signaling pathways that are important in oncogenesis. SFKs 
      can interact with tyrosine kinase receptors, such as EGFR and the VEGF receptor. 
      SFKs can affect cell proliferation via the Ras/ERK/MAPK pathway and can regulate 
      gene expression via transcription factors such as STAT molecules. SFKs can also 
      affect cell adhesion and migration via interaction with integrins, actins, 
      GTPase-activating proteins, scaffold proteins, such as p130(CAS) and paxillin, 
      and kinases such as focal adhesion kinases. Furthermore, SFKs can regulate 
      angiogenesis via gene expression of angiogenic growth factors, such as fibroblast 
      growth factor, VEGF, and interleukin 8. On the basis of these important findings, 
      small-molecule SFK inhibitors have been developed and are undergoing early phase 
      clinical testing. In preclinical studies these agents can suppress tumor growth 
      and metastases. The agents seem to be safe in humans and could add to the 
      therapeutic arsenal against subsets of cancers.
FAU - Kim, Lori C
AU  - Kim LC
AD  - University of South Florida College of Medicine, Tampa, FL, USA.
FAU - Song, Lanxi
AU  - Song L
FAU - Haura, Eric B
AU  - Haura EB
LA  - eng
PT  - Journal Article
PT  - Review
PL  - England
TA  - Nat Rev Clin Oncol
JT  - Nature reviews. Clinical oncology
JID - 101500077
RN  - 0 (Actins)
RN  - 0 (Crk-Associated Substrate Protein)
RN  - 0 (GTPase-Activating Proteins)
RN  - 0 (Integrins)
RN  - 0 (Paxillin)
RN  - 0 (Transcription Factors)
RN  - EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases)
RN  - EC 2.7.10.2 (Focal Adhesion Protein-Tyrosine Kinases)
RN  - EC 2.7.10.2 (src-Family Kinases)
RN  - EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
SB  - IM
MH  - Actins/metabolism
MH  - Animals
MH  - Cell Adhesion
MH  - Cell Movement
MH  - Cell Proliferation
MH  - Cell Survival
MH  - Clinical Trials as Topic
MH  - Crk-Associated Substrate Protein/metabolism
MH  - Drug Evaluation, Preclinical
MH  - Enzyme Activation
MH  - Extracellular Signal-Regulated MAP Kinases/metabolism
MH  - Focal Adhesion Protein-Tyrosine Kinases/metabolism
MH  - GTPase-Activating Proteins/metabolism
MH  - Gene Expression Regulation, Neoplastic
MH  - Genes, ras
MH  - Humans
MH  - Integrins/metabolism
MH  - MAP Kinase Signaling System
MH  - Neoplasm Metastasis/drug therapy
MH  - Neoplasms/*drug therapy/metabolism
MH  - Paxillin/metabolism
MH  - Protein Structure, Tertiary
MH  - Receptor Protein-Tyrosine Kinases/metabolism
MH  - Signal Transduction
MH  - Time Factors
MH  - Transcription Factors/metabolism
MH  - src-Family Kinases/antagonists & inhibitors/chemistry/*genetics/*metabolism
RF  - 104
EDAT- 2009/09/30 06:00
MHDA- 2009/12/16 06:00
CRDT- 2009/09/30 06:00
PHST- 2009/09/30 06:00 [entrez]
PHST- 2009/09/30 06:00 [pubmed]
PHST- 2009/12/16 06:00 [medline]
AID - nrclinonc.2009.129 [pii]
AID - 10.1038/nrclinonc.2009.129 [doi]
PST - ppublish
SO  - Nat Rev Clin Oncol. 2009 Oct;6(10):587-95. doi: 10.1038/nrclinonc.2009.129.