AI Article Synopsis
- The Wnt signaling pathway is often activated in cancers, and Wnt inhibitory factor-1 (WIF-1) serves as an important antagonist by binding to Wnt ligands.
- A study using methylation-specific PCR found that WIF-1 was methylated in 89.7% of 68 nasopharyngeal carcinoma (NPC) samples, while it remained unmethylated in all normal tissue samples.
- The methylation of WIF-1 is linked to the severity of cancer stages (TNM) and age, suggesting that it plays a role in activating the Wnt pathway in NPC.
Article Abstract
Activation of the wingless-type (Wnt) signaling pathway is common in cancers. The Wnt inhibitory factor-1 (WIF-1) is a secreted antagonist that acts by binding to Wnt ligands. We examined by methylation-specific PCR (MSP), whether WIF-1 is inactivated in 68 nasopharyngeal carcinomas (NPC), and 10 normal mucosa. We showed that the WIF-1 promoter was methylated in 89.7% of tumors, whereas all normal mucosa were unmethylated. The WIF-1 methylation was associated with the tumor, node, and metastasis (TNM) (p = .003) and the age (p = .014). The Wnt-5a mRNA was higher in tumors and correlated with TNM (p = .012). The methylation of WIF-1 contributes to the activation of the Wnt pathway in NPC.
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| http://dx.doi.org/10.3109/07357907.2010.494324 | DOI Listing |
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