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Compared with adjacent normal tissues, the methylation frequencies of WIF-1, RASSF1A (show RASSF1 ELISA Kits), and CDH13 (show CDH13 ELISA Kits) 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 (show RASSF1 ELISA Kits), and CDH13 (show CDH13 ELISA Kits) 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 (show CTNNB1 ELISA Kits) 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.
Reduced expression of Wif-1 and increased expression of beta-catenin (show CTNNB1 ELISA Kits) may be involved in the pathogenesis of childhood acute lymphoblastic leukemia (ALL).
Results provide evidence that WIF1 is frequently methylated in oral squamous cell carcinoma (OSCC), but not in oral submucous fibrosis tissues, which results in reduced expression. This epigenetic biomarker can be used for the early detection of OSCC.
WIF-1 down-regulation may promote tumor cells invasion and metastasis in salivary gland adenoid cystic carcinoma.
Loss of WIF1 enhances the migratory potential of glioblastoma through WNT5A that activates the WNT/Ca(2+) pathway and MALAT1.
WIF1 has a role in breast neoplasms: its inhibition significantly relieves the cancer stem cell-limiting effects of dietary compound isoliquiritigenin
Data show that the WIF domain of Wnt Inhibitory Factor 1 (WIF1) is bound by C-terminal domains of Wnt (show WNT2 ELISA Kits) proteins Wnt5a (show WNT5A ELISA Kits) and Wnt7a (show WNT7A ELISA Kits) at two sites.
Wif1 localizes to the enamel knot (show KCNK7 ELISA Kits) in which Wif1 regulates apoptosis by mediating and regulating Wnt (show WNT2 ELISA Kits)-beta-catenin (show CTNNB1 ELISA Kits) signaling. Thus, Wif1 plays an essential role in tooth development.
results demonstrate that Wif1 is not targeted for silencing by DNA methylation (show HELLS ELISA Kits) in OS. Instead, the reduced expression of Wif1 in OS cells is in context with their stage in differentiation
EZH2 (show EZH2 ELISA Kits)-induced downregulation of WIF1 expression may partially regulate Wnt (show WNT2 ELISA Kits)/beta-catenin (show CTNNB1 ELISA Kits)-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.
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 (show WNT2 ELISA Kits) 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