Article Text

  1. E. G. Thung,
  2. J. Chou,
  3. L. You,
  4. Z. Xu,
  5. D. M. Jablons
  1. University of California, San Francisco Comprehensive Cancer Center, San Francisco, CA


Nasopharyngeal carcinoma (NPC) is an epithelial tumor that is endemic to southern China. Although much is known about its pathology and its association with Epstein-Barr virus infection, the molecular events that lead to the formation of the tumor are not clearly understood. Recently, it was discovered that the up-regulation of the wingless-type (Wnt) signaling pathway may contribute to the pathogenesis of NPC. Wnt inhibitory factor-1 (WIF-1) is an antagonist of Wnt; studies have shown that WIF-1 down-regulation and the subsequent up-regulation of Wnt signaling are found in several human cancers. In order to determine if the down-regulation of WIF-1 plays a role in NPC, the expression of human WIF-1 in NPC cells was first assessed using reverse transcription-PCR. The NPC cell lines used were CNE, HNE-1, and HONE-1. The methylation status of WIF-1 was then determined by sequencing and by using methylation-specific PCR on bisulfite-treated NPC DNA. We find that WIF-1 is not expressed in NPC cells and that CpG island hypermethylation is seen in the promoter region of WIF-1, suggesting that hypermethylation silences WIF-1 expression. These results indicate that the up-regulation of the Wnt pathway due to the methylation silencing of WIF-1 is part of the mechanism that leads to tumor formation in NPC. Discovering ways to either inhibit the Wnt pathway or remove the hypermethylation of WIF-1 can thus be potentially used to therapeutically treat NPC in patients.

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