Gene interactions and pathways from curated databases and text-mining

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CDH1 — HDAC2

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
Federico et al., Cancer Res 2009 (Carcinoma, Papillary) : Chromobox protein homologue 7 protein, with decreased expression in human carcinomas, positively regulates E-cadherin expression by interacting with the histone deacetylase 2 protein ... Therefore, the ability of CBX7 to positively regulate E-cadherin expression by interacting with HDAC2 and inhibiting its activity on the E-cadherin promoter would account for the correlation between the loss of CBX7 expression and a highly malignant phenotype
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
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