RUNX3 downregulation in human lung adenocarcinoma is independent of p53, EGFR or KRAS status

Mohd Feroz Mohd Omar, Kosei Ito, Min En Nga, Ross Soo, Bee Keow Peh, Tuty Muliana Ismail, Bhavin Thakkar, Richie Soong, Yoshiaki Ito, Manuel Salto-Tellez

Research output: Contribution to journalArticlepeer-review

13 Citations (Scopus)

Abstract

RUNX3 aberrations play a pivotal role in the oncogenesis of breast, gastric, colon, skin and lung tissues. The aim of this study was to characterize further the expression of RUNX3 in lung cancers. To achieve this, a lung cancer tissue microarray (TMA), frozen lung cancer tissues and lung cell lines were examined for RUNX3 expression by immunohistochemistry, while the TMA was also examined for EGFR and p53 expression. RUNX3 promoter methylation status, and EGFR and KRAS mutation status were also investigated. Inactivation of RUNX3 was observed in 70% of the adenocarcinoma samples, and this was associated with promoter hypermethylation but not biased to EGFR/KRAS mutations. Our results suggest a central role of RUNX3 downregulation in pulmonary adenocarcinoma, which may not be dependent of other established cancer-causing pathways and may have important diagnostic and screening implications.
Original languageEnglish
Pages (from-to)783-92
Number of pages10
JournalGastric Cancer
Volume18
Issue number4
DOIs
Publication statusPublished - Oct 2012

Keywords

  • ras Proteins
  • Tumor Suppressor Protein p53
  • Receptor, Epidermal Growth Factor
  • DNA Mutational Analysis
  • Humans
  • Cell Line, Tumor
  • Proto-Oncogene Proteins
  • Tissue Array Analysis
  • DNA Methylation
  • Down-Regulation
  • Lung Neoplasms
  • Core Binding Factor Alpha 3 Subunit
  • Adenocarcinoma
  • Carcinoma, Squamous Cell
  • Immunohistochemistry
  • Mutation

ASJC Scopus subject areas

  • Cancer Research
  • Oncology
  • Pathology and Forensic Medicine

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