Yao L K, Liu G N, Huang S M, Li W T, Li Y
Department of Respiratory Medicine, First Affiliated Hospital, Guangxi Medical University, Nanning 530021, China.
Zhonghua Yi Xue Za Zhi. 2016 May 17;96(18):1410-3. doi: 10.3760/cma.j.issn.0376-2491.2016.18.005.
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.
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.
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).
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.
探讨肺癌组织中组蛋白乙酰化酶2（HDAC2）、白细胞介素-8（IL-8）、肿瘤坏死因子-α（TNF-α）的表达与吸烟之间的关系。
收集2014年4月至2015年3月在广西医科大学第一附属医院及附属肿瘤医院手术切除后经病理检查确诊的73例肺腺癌患者。所有患者均接受术前肺功能检查。用锋利刀片切取肺腺癌及癌旁组织，置于液氮中保存，取样时间小于30分钟。吸烟者定义为吸烟超过100支或每周至少有一天吸入香烟烟雾（每天超过15分钟）超过三年者。根据肺功能及是否吸烟，将肺腺癌病例分为三组：吸烟无慢性阻塞性肺疾病（COPD）组（33例）、不吸烟无COPD组（19例）、吸烟合并COPD组（21例）。采用实时聚合酶链反应（PCR）检测三组肺腺癌及癌旁组织中HDAC2、IL-8和TNF-α mRNA水平，采用蛋白质印迹法检测HDAC2蛋白表达，并进行统计学分析。
肺腺癌组织中HDAC2、IL-8和TNF-α的表达及肺腺癌的TNM分期在年龄和性别方面无显著差异（P>0.05）。与73例癌旁组织相比，肺腺癌组织中HDAC2 mRNA和蛋白水平表达显著降低（t=4.15，8.006，均P<0.01），IL-8和TNF-α mRNA水平含量升高（t=-4.252，-5.576，均P<0.01）。吸烟无COPD组和吸烟合并COPD组肺腺癌组织中HDAC2 mRNA和蛋白表达显著低于不吸烟无COPD组（0.38±0.11，0.35±0.12 vs 0.45±0.10和0.26±0.09，0.24±0.06 vs 0.33±0.10；均P<0.05），且在吸烟合并COPD组中表达最低。吸烟无COPD组和吸烟合并COPD组肺腺癌组织中IL-8和TNF-α mRNA水平显著高于不吸烟无COPD组（0.96±0.19，1.10±0.18 vs 0.71±0.13和0.62±0.21，0.64±0.20 vs 0.45±0.14；均P<0.05），且在吸烟合并COPD组中上调更明显。吸烟组（吸烟无COPD组和吸烟合并COPD组）肺腺癌的TNM分期高于不吸烟组（不吸烟无COPD组）（P=0.038）。
肺腺癌组织中HDAC2下调，IL-8、TNF-α上调。它们受吸烟影响，尤其是合并慢性阻塞性肺疾病时。
