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CDH1 — HDAC1
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Peinado et al., Mol Cell Biol 2004
:
Here we show that mammalian Snail
requires histone deacetylase (HDAC) activity to repress
E-cadherin promoter and that treatment with trichostatin A (TSA) is sufficient to block the repressor effect of Snail
Alpatov et al., Mol Cell Biol 2004
:
Nuclear speckle associated protein Pnn/DRS binds to the transcriptional corepressor CtBP and relieves
CtBP mediated repression of the
E-cadherin gene
Witta et al., Cancer Res 2006
(Carcinoma, Non-Small-Cell Lung...) :
The zinc finger transcriptional repressor, ZEB1,
inhibits E-cadherin expression by recruiting
histone deacetylases (HDAC)
Villar et al., Infect Immun 2007
(Candidiasis, Oral) :
Mucosal tissue invasion by Candida albicans is associated with
E-cadherin degradation,
mediated by transcription factor Rim101p and protease
Sap5p
Iacopino et al., Int J Oncol 2008
(Prostatic Neoplasms) :
The goal of this study was to assess the
effects of an
HDAC inhibitor, valproic acid ( VA ), on proliferation, androgen-sensitivity, androgen receptor levels and
E-cadherin ( E-cad ) expression in human prostate cancer cells
Thomas et al., Bioorg Med Chem 2008
(Lung Neoplasms) :
Prodrug incubation with beta-glucuronidase in the culture media led efficiently to the release of the parent drug and thereby restoring its ability to decrease cell proliferation, to inhibit
HDAC and to
induce E-Cadherin expression
von Burstin et al., Gastroenterology 2009
(Lung Neoplasms...) :
E-cadherin regulates metastasis of pancreatic cancer in vivo and is
suppressed by a
SNAIL/HDAC1/HDAC2 repressor complex ... In line, mesenchymal pancreatic cancer specimens and primary cell lines from genetically engineered Kras ( G12D ) mice showed
HDAC dependent down-regulation of
E-cadherin and high metastatic potential
Yamaguchi et al., Cancer Sci 2010
(Gallbladder Neoplasms) :
In TGBC2TKB cells, the expression of EZH2 and
HDAC1/2 were decreased by SAHA treatment, and p16(INK4a),
E-cadherin , and p21were simultaneously
activated ; however, no such findings were obtained in HGECs, suggesting that the effect of SAHA depends on the EZH2 mediated tumor suppressor loss ... In TGBC2TKB cells, the expression of EZH2 and
HDAC1/2 were decreased by SAHA treatment, and p16(INK4a),
E-cadherin , and p21were simultaneously
activated ; however, no such findings were obtained in HGECs, suggesting that the effect of SAHA depends on the EZH2 mediated tumor suppressor loss
Kakihana et al., J Thorac Oncol 2009
(Carcinoma, Non-Small-Cell Lung...) :
Induction of
E-cadherin in lung cancer and interaction with growth suppression by
histone deacetylase inhibition ... In contrast to H460 and H661, H157 cells were resistant to
E-cadherin up-regulation by
HDAC inhibitors
Lin et al., Oncogene 2010
:
In the absence of
LSD1 , Snai1 fails to
repress E-cadherin
Lei et al., Int J Biochem Cell Biol 2010
:
The data also suggest that the
repression of transcription of ZO-1 and
E-cadherin by
HDAC1 may be involved in TGF-beta1 induced EMT
Huang et al., Mol Pharmacol 2011
:
This finding, together with the
HDAC inhibitor
induced up-regulation of KLF4 and
E-cadherin , suggests that HDAC inhibitors could activate the expression of these genes through changes in histone methylation status ... This finding, together with the
HDAC inhibitor
induced up-regulation of KLF4 and
E-cadherin , suggests that HDAC inhibitors could activate the expression of these genes through changes in histone methylation status
Suda et al., J Thorac Oncol 2011
(Adenocarcinoma...) :
We also found that the
histone deacetylase inhibitor, MS-275,
restored E-cadherin expression and moderate sensitivity to erlotinib in HCC4006ER cells, on the other hand, transforming growth factor beta, an inducer of EMT, led to moderate erlotinib resistance in HCC4006 parental cells
Yi et al., Chemotherapy 2012
(Carcinoma...) :
DNMT inhibitors and
HDAC inhibitors
regulate E-cadherin and Bcl-2 expression in endometrial carcinoma in vitro and in vivo
Nagathihalli et al., Mol Cancer Ther 2012
(Carcinoma, Non-Small-Cell Lung...) :
Smoking induces epithelial-to-mesenchymal transition in non-small cell lung cancer through
HDAC mediated downregulation of
E-cadherin
Iordache et al., International journal of molecular sciences 2012
:
RT-PCR assay showed that
HDAC inhibitors
down-regulated the expression of endothelial genes such as
VE-cadherin , CD133, CXCR4 and Tie-2