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Epigenetic inactivation of TSLC1 gene in nasopharyngeal carcinoma

Angela Bik-Yu Hui1, Kwok-Wai Lo, Joseph Kwong

  • 1Department of Anatomical and Cellular Pathology, The Chinese University of Hong Kong, Hong Kong, China.

Molecular Carcinogenesis
|November 26, 2003
PubMed

Insights

The TSLC1 gene, a tumor suppressor, is frequently inactivated by promoter hypermethylation in nasopharyngeal carcinoma (NPC). This epigenetic silencing of TSLC1 contributes to NPC development, highlighting its role in this endemic cancer.

Area of Science:

  • Oncology
  • Genetics
  • Epigenetics

Background:

  • 11q23 deletions are common in nasopharyngeal carcinoma (NPC).
  • TSLC1 (tumor suppressor in lung cancer) is a candidate tumor suppressor gene located at 11q23.
  • TSLC1 inactivation via promoter hypermethylation is observed in lung, liver, and breast cancers.

Purpose of the Study:

  • To investigate the role of the TSLC1 gene in NPC tumorigenesis.
  • To screen for mutations and aberrant methylation of TSLC1 in NPC samples.

Main Methods:

  • Screening of 5 NPC cell lines, 3 NPC xenografts, and 38 primary NPC cases for TSLC1 mutations and methylation.
  • Bisulfite sequencing to detect TSLC1 promoter methylation.
  • Treatment of NPC cell lines with 5-aza-2'-deoxycytidine to assess gene expression restoration.

Main Results:

  • No somatic mutations of TSLC1 were detected, except for one 9-bp deletion in exon 8 in a primary NPC sample.
  • Aberrant methylation of the TSLC1 promoter was found in 4 NPC cell lines, correlating with loss of TSLC1 expression.
  • TSLC1 expression was restored upon treatment with a demethylating agent.
  • TSLC1 promoter hypermethylation was observed in 34.2% of primary NPCs, but not in normal nasopharyngeal epithelia.

Conclusions:

  • TSLC1 gene expression is frequently silenced by promoter hypermethylation in NPC.
  • Epigenetic inactivation of TSLC1 is a significant event in NPC tumorigenesis.
  • TSLC1 is a target tumor suppressor gene in this endemic cancer.

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