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DACH1 expression is decreased in glomerulopathy imply a potential role for DACH1 in the this development of human chornic glomerulopathy.
Knockdown of DACH1 expression can remarkably enhance the cell apoptosis, restrain the proliferation, migration and invasion of Capan-1 cells.
DACH1 expression regulates the pancreatic cancer cell apoptosis.
Low DACH1 expression is associated with invasion of lung adenocarcinoma.
This study concludes that MiR-217 is the upstream regulator of PGC-1alpha in breast cancer regulation in vitro, possibly independent of DACH1 signaling pathway.
Kaplan-Mier analysis of human NSCLC samples demonstrated that high DACH1 mRNA levels predicted favorable prognosis for relapse-free and overall survival. In agreement, high CXCL5 expression predicted a worse prognosis for survival.
DACH1 expression was reduced in hepatocellular carcinoma even at early stage and associated with tumor progression. Overexpression inhibited HCC cell growth and migration by inactivating the Wnt pathway via GSK3beta phosphorylation to suppress beta-catenin.
In breast cancer, some GATA3 effects shift from tumor suppressing to tumor promoting during tumorigenesis, with deregulation of three genes, BCL2, DACH1, THSD4, representing major GATA3-controlled processes in cancer progression.
Results indicated that DACH1 was a novel molecular marker of RCC and it attributed to the malignant behavior of renal cancer cells.
Data indicate that dachshund family transcription factor 1 (DACH1) suppresses gastric cancer cell proliferation, invasion and metastasis by inhibiting transforming growth factor beta (TGF-beta) signalling pathways both in vitro and in vivo.
results suggest that DACH1 loss of function results in increased cell growth, motility and invasiveness through TGF-beta-mediated EMT, and DACH1 loss of function has important therapeutic implications for targeted therapies of CRC
DACH1 is a determinant of benign and malignant prostate epithelium cellular growth, migration, and cytokine abundance in vivo.
Further evaluation of the methylation of DACH1, DKK1, and WIF1 in a clinical patient group confirmed the frequent methylation of WIF1 and intermediate or low frequency of methylation of DACH1 or DKK1, respectively.
DACH1 inhibits aldosterone secretion in human adrenals, and transforming growth factor-beta signaling pathway is activated in DACH1 overexpressed cells and may mediate inhibition of aldosterone secretion in human adrenals.
Familial young-onset diabetes, pre-diabetes and cardiovascular disease are associated with genetic variants of DACH1 in Chinese
Nuclear DACH1 expression appears to be a Luminal A biomarker predictive of good prognosis, but is not independent of clinical stage, tumour size, NPI status or systemic therapy.
DACH1 is frequently methylated in human colorectal cancers (CRC) and methylation of DACH1 may serve as detective and prognostic marker in CRC.
Cell fate factor DACH1 represses YB-1-mediated oncogenic transcription and translation.
DACH1 binds p53 to inhibit NSCLC cellular growth.
DACH1 gene promoter methylation could lead to a decrease or absence of DACH1 expression in endometrial carcinoma.
DACH1 stimulates coronary artery growth by activating Cxcl12 expression and endothelial cell migration against blood flow into developing arteries
HDAC4-mediated SUMOylation of the corepressor DACH1 is decreased, which protects DACH1 from proteasomal degradation
The results of this study suggested the involvement of the mouse Dach1 gene in adult neurogenesis; cells expressing this gene exhibit the properties of adult NSCs or neuroblasts and respond to MCAo by enhanced neurogenesis.
find that in cells growing in IGF-1 (and unresponsive to EGF), DACH1 is devoid of tumor suppressor activity
The mouse dachshund gene is related to the Ski proto-oncogene and is expressed in eye and limb.
In the mouse, Dach1 expression in the developing ear also overlaps with the expression of Eya1 (an eya homologue)
D6 enhancer exerts highly tissue-specific activity in neurons of the neocortex and hippocampus and in neural stem cells.
Dach1 is a target gene of FGF signaling during limb skeletal development, and Dach1 may function as an intermediary in the FGF signaling pathway regulating cell proliferation or differentiation
Dach1 is critical for postnatal survival of mice
The phosphatase function of Eya switches the function of Six1-Dach from repression to activation, causing transcriptional activation through recruitment of co-activators
The Pax-Eya-Six-Dach network is at best only partly conserved during lens and nasal placode development.
DACH1 repressed cyclin D1 through a novel mechanism via a c-Jun DNA-binding partner, requiring the DACH1 alpha-helical DS domain which recruits corepressors to the local chromatin.
These studies demonstrate a novel mechanism by which DACH1 blocks c-Jun-mediated contact-independent growth through repressing the c-Jun delta domain.
With Dach2, may redundantly control female reproductive tract formation by regulating expression of target genes required for development of the Mullerian duct.
These data identify a pathway by which an endogenous cell-fate determination factor blocks oncogene-dependent tumor metastasis via a key heterotypic mediator.
This gene encodes a chromatin-associated protein that associates with other DNA-binding transcription factors to regulate gene expression and cell fate determination during development. The protein contains a Ski domain that is highly conserved from Drosophila to human. Expression of this gene is lost in some forms of metastatic cancer, and is correlated with poor prognosis. Multiple transcript variants encoding different isoforms have been found for this gene.
dachshund homolog 1
, dachshund homolog 1 (Drosophila)
, dachshund 1
, dachshund protein
, dachshund homolog 1-like