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Human WIF1 Protein expressed in Wheat germ - ABIN1325330
Kansara, Tsang, Kodjabachian, Sims, Trivett, Ehrich, Dobrovic, Slavin, Choong, Simmons, Dawid, Thomas: Wnt inhibitory factor 1 is epigenetically silenced in human osteosarcoma, and targeted disruption accelerates osteosarcomagenesis in mice. in The Journal of clinical investigation 2009
WIF1 methylation may serve as a potential prognostic marker for patients with chondrosarcoma.
our findings indicate that HOXC6 plays an important role in the progress and prognosis of human glioma and promotes glioma U87 cell growth through the WIF-1/Wnt signaling pathway
Data revealed that the upregulation of WIF1 induced autophagy in non-small cell lung cancer (NSCLC) cells. WIF1-mediated autophagy was demonstrated to inhibit Wnt/betacatenin signaling by downregulating Dvl2, which contributed to the inhibition of the proliferation and the promotion of the apoptosis of NSCLC cells.
WIF-1 gene methylation is associated with pathogenesis of multiple human tumors.
the expression of WIF-1 was low in GBC cells due to aberrant hypermethylation of its promoter region. Additionally, an alternative pathogenesis of GBC was indicated in which c-Jun causes hypermethylation of the WIF-1 promoter region, and represses the expression of WIF-1 through transcriptional regulation and interaction with DNMT1 as an early event in the tumorigenesis of GBC.
miR-590-3p regulates colon cancer progression via WIF1 and DKK1, which suggests that miR-590-3p may be a promising candidate for therapeutic applications in colon cancer treatment
We identify a loss-of-function mutation in WIF1 (NM_007191 p.W15*), which is involved in mesoderm segmentation, as the suspected cause of the Nail-Patella-like disorder observed in this family.
the results of our study show that down-regulated INTS6 expression is associated with a poorer prognosis in hepatocellular carcinoma (HCC) patients. This newly identified INTS6/WIF-1 axis indicates the molecular mechanism of HCC and may represent a therapeutic target in HCC patients.
the promoters of WIF1, NLK, and APC are highly methylated in the nasopharyngeal cancers (NPC) and gastric carcinoma (GC) cell lines, and the 3 genes are also regulated by miR-BART19-3p expressed by Epstein-Barr virus (EBV); expression of the WIF1, APC, and NLK genes is strongly affected by hypermethylation, and in EBV-associated tumors, the 3 genes are also affected by miR-BART19-3p
Data show the frequency of WIF-1 hypermethylation significantly increased in non-small cell lung cancer (NSCLC) specimens compared with normal lung tissue. WIF-1 hypermethylation is predominant in squamous cell carcinoma (SCC), suggesting that WIF-1 methylation contributes to the development of NSCLC, especially SCC. [review]
Study supported the hypothesis that Wnt inhibitory factor 1 (WIF1) is crucial as a negative regulator of the functions of endothelial cells in angiogenesis and that hypoxia plays an important role in controlling WIF1 expression and angiogenesis.
Our data suggests that total cellular b-catenin levels decrease in the presence of secreted frizzled-related protein 1 and Wnt inhibitory factor 1, and a significant increase in cell death after tyrosine kinase inhibitor treatment is observed. On the contrary, when secreted frizzled-related protein 1 is suppressed, total b-catenin levels increase in the cell and the cells become resistant to tyrosine kinase inhibitors.
Gallbladder cancer patients with hypermethylated WIF-1 exhibited worse overall survival than those with hypomethylated WIF-1.
In astrocytoma specimens, tumor areas with numerous single cells were identified which strongly express Wif-1.
Hypermethylation of WIF1 (WNT inhibitory factor 1) and NPY (neuropeptide Y) genes was significantly higher in tumor tissue compared to normal tissue, independently of tumor stage.
the expression levels of WIF-1 were low in gallbladder cancer tumor tissues and the GBC-SD, SGC-996 and NOZ gallbladder cancer cell lines. This low expression was associated with the methylation status of the WIF-1 gene promotor.
Compared with adjacent normal tissues, the methylation frequencies of WIF-1, RASSF1A, and CDH13 genes were significantly higher but the mRNA levels of these 3 genes were significantly lower in EC tissues. The survival rates of patients with WIF-1, RASSF1A, and CDH13 methylations were significantly lower than those of patients without methylation
Promoter hypermethylation WIF1 play an important role in the carcinogenesis of lung cancer.
HOTAIR can affect the radiosensitivity of pancreatic ductal adenocarcinoma (PDAC) cells partly via regulating the expression of WIF-1, and HOTAIR-WIF-1 axis is a potential target for PDAC radiotherapy.
beta-catenin expression may also be a poor prognostic factor for cervical cancer (CC) while WIF1 could be a potential drug target for treatment of advanced CC.
Wif1 localizes to the enamel knot in which Wif1 regulates apoptosis by mediating and regulating Wnt-beta-catenin signaling. Thus, Wif1 plays an essential role in tooth development.
WIF1 has a role in breast neoplasms: its inhibition significantly relieves the cancer stem cell-limiting effects of dietary compound isoliquiritigenin
results demonstrate that Wif1 is not targeted for silencing by DNA methylation in OS. Instead, the reduced expression of Wif1 in OS cells is in context with their stage in differentiation
EZH2-induced downregulation of WIF1 expression may partially regulate Wnt/beta-catenin-dependent crypt hyperplasia in response to citrobacter rodentium infection
Dysregulation of this endodermal Shh-Wif1-b-catenin signaling axis contributes to ARM pathogenesis.
It is anticipated that our findings will contribute to expansion of our understanding of WIF1 biological function on heart development and possible modes of treatment of heart diseases
WIF1 secretion by the Mullerian duct mesenchyme plays a role in Mullerian duct regression in fetal males
These data suggest that WIF-1 may take part in the fine-tuning of cartilage and bone turnover, promoting the balance of cartilage versus bone anabolism.
Wnt inhibitory factor 1 (Wif1) is regulated by androgens and enhances androgen-dependent prostate development
Osteoblastic Wif1 overexpression disrupts stem cell quiescence, leading to a loss of self-renewal potential.
wif1 is a modulator of cardiomyocyte differentiation
a novel regulatory loop of Bmp4-Smad1-Wif1-Wnt/beta-catenin in coordinating BMP and Wnt pathways to control fetal lung development
These results identify Wif-1 as a novel extracellular Wnt modulator in cartilage biology.
WIF-1 protein inhibits rod production, and anti-WIF-1 antibodies increase rod production; in contrast, Wnt4 promotes rod production.
Dkk-1/Wnt/beta-catenin cascade may mediate the proliferation and migration of hepatocellular carcinoma cells during the metastasis process.
Wif1 mRNA can be detected as early as the developmental stage E11, and expression persists to adulthood.
Data provided a full expression pattern for Wif1 in limb development, for which no limb expression had been documented so far.
Results indicate that WIF-1 plays as a negative regulator of osteoblastic differentiation in mouse mesenchymal C3H10T1/2 cells in vitro.
targeted deletion of Wif1 accelerated development of radiation-induced osteosarcomas in vivo
In an examination of signaling pathways in developing Xenopus lung, wif1 was expressed in the mesenchyme layer of the entire lungs through stages 39-41.
Data describe the importance of proper level of Wnt signaling for normal development of swimbladder in Wif1 morphant zebrafish.
The protein encoded by this gene functions to inhibit WNT proteins, which are extracellular signaling molecules that play a role in embryonic development. This protein contains a WNT inhibitory factor (WIF) domain and five epidermal growth factor (EGF)-like domains, and is thought to be involved in mesoderm segmentation. This gene functions as a tumor suppressor gene, and has been found to be epigenetically silenced in various cancers.
, wnt inhibitory factor 1
, WNT inhibitory factor 1
, wnt inhibitory factor 1-like
, Wnt inhibitory factor-1
, wnt inhibitory factor-1