Objective: To investigate the relationship between the expression of histone acetylation enzyme 2 (HDAC2), interleukin-8 (IL-8), tumor necrosis factor-α (TNF-α) in lung adenocarcinoma tissues and smoking.
Methods: A total of 73 cases of lung adenocarcinoma confirmed by pathological examination after surgical removals were collected in the First Affiliated Hospital and Affiliated Tumor Hospital of Guangxi Medical University from April 2014 to March 2015. All patients received preoperative lung function test. Lung adenocarcinoma and para-cancer tissues were cut by the sharp blade and stored in liquid nitrogen and the sampling time was less than 30 minutes. Smokers were defined as people who had smoked more than 100 cigarettes or inhaled the smoke of cigarettes at least one day a week (more than 15 minutes every day) more than three years. According to the lung function and whether smoking or not, the cases of lung adenocarcinoma were divided into three groups: smoking without chronic obstructive pulmonary disease (COPD) group (33 cases), without smoking and COPD group (19 cases), smoking with COPD group (21 cases). The levels of HDAC2, IL-8 and TNF-α mRNA in lung adenocarcinoma and para-cancer tissues of groups were detected by real-time polymerase chain reaction (PCR) and the expression of HDAC2 protein was detected by Western blotting, and statistical analysis was carried out.
Results: The expression of HDAC2, IL-8 and TNF-α in lung adenocarcinoma tissues and TNM stage of lung adenocarcinoma showed no significant differences with respect to age and gender (P>0.05). Compared with the para-cancer tissues of 73 cases, the expression of HDAC2 at mRNA and protein levels in lung adenocarcinoma tissues were significantly lower (t=4.15, 8.006, all P<0.01). and the content of IL-8 and TNF-α at mRNA levels were increased (t=-4.252, -5. 576, all P<0.01). The expression of HDAC2 mRNA and protein in lung adenocarcinoma tissues in smoking without COPD group and smoking with COPD group were significantly lower than in without smoking and COPD group (0.38±0.11, 0.35±0.12 vs 0.45±0.10 and 0.26±0.09, 0.24±0.06 vs 0.33±0.10; all P<0.05), and it was the lowest expression in smoking with COPD group. IL-8 and TNF-α at mRNA levels in lung adenocarcinoma tissues in smoking without COPD group and smoking with COPD group were significantly higher than in without smoking and COPD group (0.96±0.19, 1.10±0.18 vs 0.71±0.13 and 0.62±0.21, 0.64±0.20 vs 0.45±0.14; all P<0.05), and the up-regulation was more obvious in smoking with COPD group. The TNM stage of lung adenocarcinoma in smoking group (smoking without COPD group and smoking with COPD group) was higher than without smoking group (without smoking and COPD group)(P=0.038).
Conclusion: HDAC2 is down-regulated and IL-8, TNF-α are up-regulated in lung adenocarcinoma tissues. They are influenced by smoking and especially when combined with chronic obstructive pulmonary disease.