Abstract
We previously reported that patients with lung adenocarcinomas with KRAS gene mutations and strong proliferating activity had poorer outcomes, even in the early stage of the disease. The aim of the present study was to elucidate the potential molecular basis of these highly malignant lung tumors by focusing on S100 proteins (S100A2, S100A7, and S100A11), which are downstream targets of oncogenic KRAS and promoters of tumor progression. The immunohistochemical expression of S100 proteins was examined in 179 primary lung adenocarcinomas, and the potential relationships between their levels and clinicopathologic factors were analyzed. Among the three subtypes, S100A11 levels were significantly higher in adenocarcinomas with KRAS mutations and strong proliferating activity. They were also higher in adenocarcinomas with poorly differentiated tumors. Furthermore, higher levels of S100A11 were associated with shorter disease-free survival. These results suggest that the up-regulation of S100A11 plays a role in tumor progression, particularly in KRAS-mutated lung adenocarcinomas.
Highlights
Lung cancer is one of the most common causes of cancer-related death in the developed world [1,2]
We previously reported that patients with lung adenocarcinomas with KRAS gene mutations and strong proliferating activity had poorer outcomes, even in the early stage of the disease [6]
S100A11 levels were significantly higher in adenocarcinomas with KRAS mutations and strong proliferating activity (P = 0.038 in the Kruskal-Wallis test, Fig 3)
Summary
Lung cancer is one of the most common causes of cancer-related death in the developed world [1,2]. A large proportion of patients, even those with early stage non-small-cell lung cancer, die due to recurrent disease [3,4]. Some lung tumors are sensitive to conventional chemotherapeutic agents or certain molecular targeting agents, many are not [5,6]. A deeper understanding of the molecular basis of lung carcinogenesis is needed in order to develop novel therapeutic strategies. We previously reported that patients with lung adenocarcinomas with KRAS gene mutations and strong proliferating activity had poorer outcomes, even in the early stage of the disease [6]. The aim of the present study was to elucidate the potential molecular basis
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