Relative low expression of large tumor suppressor 2 (LATS2) gene in EGFR-mutated pulmonary adenocarcinomas from non-smokers

Abstract

BACKGROUND AND AIM OF STUDY: Large Tumor Suppressor 2 (LATS2) is a new putative tumor suppressor gene which is involved in different signaling pathways including Hippo, p53, Ras and Akt networks. Some of these pathways overlap with those downstream signaling pathways of Epidermal Growth Factor Receptor (EGFR) gene. The regulated expression of LATS2 plays a signifi cant role in cell proliferation and apoptosis. Loss of LATS2 expression and hence its putative tumor suppressor function may result in genetic instability and promote tumor cell growth. The aim of this study was to investigate the expression status of LATS2 in lung Adenocarcinomas (AD) in relation to gender, smoking status as well as EGFR mutation status METHODS: Total RNA was extracted from resected pulmonary adenocarcinomas and was reversely transcribed into cDNA. Real-time PCR with SYBR Green I method was used to assess the relative expression levels of LATS2 in lung AD with ribosomal 18S gene as the endogenous reference gene. The EGFR mutation status was analyzed by sequencing. RESULTS: 50 lung AD were included (M : F = 23:27, smoker : non-smoker = 19:31, TNM Stages I/II/III/IV = 29/12/8/1). There was no signifi cant difference in the expression of LATS2 between genders. However, LATS2 expression was higher in non-smokers than in current or ex-smokers (p = 0.041). Among non-smokers, LATS2 expression was also signifi cantly lower in those AD bearing EGFR mutations (n = 13) compared to AD that were EGFR wild-type (n = 18) (p = 0.037). CONCLUSION: LATS2 showed differential expression between AD from smokers and from non-smokers. The potential relationship or interaction between relatively low LATS2 expression and EGFR mutation status in pulmonary AD from non-smokers deserves further investigation.