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:3.1.3.16 (
calcineurin
)
17,112
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Lung cancer is the number 1 cause of cancer-related casualties in the world. Appropriate diagnostic markers and novel targets for lung cancer are needed. Chitooligosaccharide deacetylase homolog (
YDJC
) catalyzes the deacetylation of acetylated carbohydrates; however, the role of
YDJC
in lung cancer progression has yet to be studied. A549 lung cancer orthotopic mouse model was used for mice experiments. We found that
YDJC
overexpression contributes to lung cancer progression in an orthotopic mouse model. Long-term treatment (48 h) induces
YDJC
expression in sphingosylphosphorylcholine (SPC)-induced epithelial-mesenchymal transition (EMT). Gene silencing of
YDJC
(siYDJC) reduced N-cadherin expression and increased E-cadherin expression in SPC-induced EMT. Overexpression of
YDJC
reverses them but overexpression of the deacetylase deficient mutant
YDJC
D13A
could not. Interestingly, overexpression of CDC16, a
YDJC
binding partner, suppressed EMT. ERK2 is activated in siCDC16-induced EMT.
YDJC
overexpression reduces expression of protein phosphatase 2A (
PP2A
), whereas CDC16 overexpression induces
PP2A
expression.
YDJC
overexpression induced ubiquitination of
PP2A
but
YDJC
D13A
could not. CDC16 overexpression increased the ubiquitination of
YDJC
. These results suggest that
YDJC
contributes to the progression of lung cancer via enhancing EMT by inducing the ubiquitination of
PP2A
. Therefore,
YDJC
might be a new target for antitumor therapy against lung cancer.
...
PMID:YDJC Induces Epithelial-Mesenchymal Transition via Escaping from Interaction with CDC16 through Ubiquitination of PP2A. 3148 24
