Wnt signaling activation and WIF-1 silencing in nasopharyngeal cancer cell lines

  • Yu Ching Lin
  • , Liang You
  • , Zhidong Xu
  • , Biao He
  • , Iwao Mikami
  • , Elaine Thung
  • , Josephine Chou
  • , Kristopher Kuchenbecker
  • , Jae Kim
  • , Dan Raz
  • , Cheng Ta Yang
  • , Jan Kan Chen
  • , David M. Jablons*
  • *Corresponding author for this work

Research output: Contribution to journalJournal Article peer-review

62 Scopus citations

Abstract

Aberrant activation of Wingless-type (Wnt) signaling pathway plays a critical role in oncogenesis of various human cancers. Wnt inhibitory factor-1 (WIF-1) is a secreted antagonist of Wnt signaling and acts through direct binding to Wnt in the extracelllular space. Recently, we reported Wnt signaling in various human malignancies. In addition, we identified in lung cancer that WIF-1 is silenced due to promoter hypermethylation. In this study, we found constitutive activation of Wnt signaling and WIF-1 silencing in nasopharyngeal carcinoma (NPC) cell lines. Furthermore, by utilizing methylation-specific PCR and sequence analysis, we demonstrated that frequent hypermethylation of the WIF-1 promoter correlates with WIF-1 silencing in NPC cell lines. Our results indicate that aberrant Wnt signaling is a common event in NPC carcinogenesis linked with WIF-1 silencing in at least cell lines. Strategies targeting these molecules should be potentially promising in treating NPC.

Original languageEnglish
Pages (from-to)635-640
Number of pages6
JournalBiochemical and Biophysical Research Communications
Volume341
Issue number2
DOIs
StatePublished - 10 03 2006

Keywords

  • Nasopharyngeal carcinoma
  • Promoter hypermethylation
  • Transfection
  • Wnt inhibitory factor-1
  • Wnt signaling

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