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:3.2.1.23 (
beta-galactosidase
)
14,648
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Loss of
ABI gene family member 3-binding protein
(
ABI3BP
) expression may be functionally involved in the pathogenesis of cancer. Previous reports have indicated a loss of expression in lung cancer and a presumed role in inducing cellular senescence. We show here that
ABI3BP
expression is significantly decreased in most malignant thyroid tumors of all types. To better understand
ABI3BP
's role, we created a model by re-expressing
ABI3BP
in two thyroid cancer cell lines. Re-expression of
ABI3BP
in thyroid cells resulted in a decrease in transforming activity, cell growth, cell viability, migration, invasion, and tumor growth in nude mice.
ABI3BP
re-expression appears to trigger cellular senescence through the p21 pathway. Additionally,
ABI3BP
induced formation of heterochromatin 1-binding protein gamma-positive senescence-associated (SA) heterochromatin foci and accumulation of SA
beta-galactosidase
. The combination of a decrease in cell growth, invasion, and other effects upon
ABI3BP
re-expression in vitro helps to explain the large reduction in tumor growth that we observed in nude mice. Together, our data provide evidence that the loss of
ABI3BP
expression could play a functional role in thyroid tumorigenesis. Activation of
ABI3BP
or its pathway may represent a possible basis for targeted therapy of certain cancers.
...
PMID:Re-expression of ABI3-binding protein suppresses thyroid tumor growth by promoting senescence and inhibiting invasion. 1855 58
A novel
target of NESH-SH3
(
TARSH
) was identified as a cellular senescence related gene in mouse embryonic fibroblasts (MEFs) replicative senescence, the expression of which has been suppressed in primary clinical lung cancer specimens. However, the molecular mechanism underlying the regulation of
TARSH
involved in pulmonary tumorigenesis remains unclear. Here we demonstrate that the reduction of
TARSH
gene expression by short hairpin RNA (shRNA) system robustly inhibited the MEFs proliferation with increase in senescence-associated
beta-galactosidase
(SA-beta-gal) activity. Using p53-/- MEFs, we further suggest that this growth arrest by loss of
TARSH
is evoked by p53-dependent p21(Cip1) accumulation. Moreover, we also reveal that
TARSH
reduction induces multicentrosome in MEFs, which is linked in chromosome instability and tumor development. These results suggest that
TARSH
plays an important role in proliferation of replicative senescence and may serve as a trigger of tumor development.
...
PMID:Implication of p53-dependent cellular senescence related gene, TARSH in tumor suppression. 1933 57
