Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:2.7.10.2 (
focal adhesion kinase
)
44,029
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Colorectal cancer (CRC) is one of the most common malignancies in the world. Emerging evidence has shown that dysregulation of tripartite motif (TRIM) family proteins is strongly correlated with the tumorigenesis of CRC. Here, we evaluated the biological roles of
TRIM66
, a member of TRIM family, in the progression of CRC. The results demonstrated that
TRIM66
was markedly up-regulated in both CRC tissues and cell lines. To further investigate the functions of
TRIM66
in CRC, CRC cells were infected with lentivirus expressing anti-
TRIM66
shRNA (sh-
TRIM66
) or control lentivirus (sh-con). We found that knockdown of
TRIM66
significantly inhibited cell proliferation, migration, invasion of CRC cells.
TRIM66
knockdown also suppressed epithelial-mesenchymal transition (EMT), as proved by the increased E-cadherin expression and decreased expressions of N-cadherin and vimentin. Furthermore,
TRIM66
knockdown markedly inhibited tumor growth in a mouse xenograft model. Knockdown of
TRIM66
reduced the activation of
JAK2
/STAT3 signaling pathway in CRC cells. Treatment with AG490, an inhibitor of
JAK2
/STAT3 signaling pathway, enhanced the inhibitory effects of
TRIM66
knockdown on cell proliferation, migration and invasion. These findings suggested that knockdown of
TRIM66
exhibited anti-tumor activity through inhibiting the
JAK2
/STAT3 signaling pathway in CRC cells.
...
PMID:Knockdown of TRIM66 inhibits cell proliferation, migration and invasion in colorectal cancer through JAK2/STAT3 pathway. 3147 44
