Few studies have examined the effect of individual counseling for smoking cessation in China. The present study evaluated the efficacy of individual counseling in patients with chronic obstructive pulmonary disease (COPD) and asymptomatic smokers. This prospective randomized study evaluated 85 smokers with COPD and 105 asymptomatic smokers with normal lung function. The individuals were randomly allocated to intervention and control groups. Subjects in the intervention group were provided with individual cognitive counseling based on face-to-face individual consultation, self-help materials and nine telephone follow-ups. Subjects in the control group were provided with simple smoking cessation advice. The smoking status for all subjects and the St. George’s Respiratory Questionnaire (SGRQ) for COPD patients were assessed at baseline, week 4 and month 6. The COPD patient exacerbations during the 6 months were recorded. In the total study population, individual counseling resulted in higher abstinence rates compared with those in the control: Intervention vs. control, 23.4 vs. 10.4% (P=0.007), respectively. Similar results were observed in the smokers with COPD: Intervention vs. control, 40.5 vs. 18.6% (P=0.027), respectively. However, for asymptomatic smokers, the effect of individual counseling was identified to be statistically insignificant: Intervention vs. control, 9.6 vs. 3.8% (P=0.230), respectively. SGRQ scores and COPD exacerbations were significantly improved in patients who abstained from smoking compared with those in the patients who failed to stop smoking. Airway obstruction, quitting motivation and individual counseling were predictors associated with smoking cessation. Airway obstruction was the most significant predictor of smoking cessation (odds ratio, 4.215; 95% confidence interval, 2.215–7.865). The results of the present study show that individual counseling is an effective method for smoking cessation, particularly in COPD patients. However, its efficacy in asymptomatic smokers requires confirmation in further studies.

In this study, we aimed to explore the long noncoding RNA expression pattern in squamous cell lung cancer (SQCC) on a genome-wide scale. Total RNAs were extracted from 16 lung SQCC patients’ normal and matched lung cancer tissues by Trizol reagent. The expression level of genome-wide scale lncRNA and mRNA was determined by microarray. qRT-PCR was used to validate the lncRNA expression level in 47 patients. Data analyses were performed using R and Bioconductor. A total of 2,748 up and 852 down regulated probes were identified to be significantly and differentially expressed in tumor tissues. The annotation result of their co-expressed mRNAs showed that the most significantly related category of GO analysis was development and differentiation, while the most significantly related pathway was cell cycle. Subgroup analysis identified that 46 and 18 probes were specifically differentially expressed in smoking and moderately differentiated tumors, respectively. Our study indicated that clusters of lncRNAs were significantly and differentially expressed in SQCC compared with normal tissues in the same subject. They may exert a significant role in lung cancer development and could be potential targets for future treatment of SQCC.

The Ras-related C3 botulinum toxin substrate 1 (RAC1), a member of the Rho family of small guanosine triphosphatases, is critical for many cellular activities, such as phagocytosis, adhesion, migration, motility, cell proliferation, and axonal growth. In addition, RAC1 plays an important role in cancer angiogenesis, invasion, and migration, and it has been reported to be related to most cancers, such as breast cancer, gastric cancer, testicular germ cell cancer, and lung cancer. Recently, the therapeutic target of RAC1 in cancer has been investigated. In addition, some investigations have shown that inhibition of RAC1 can reverse drug-resistance in non-small cell lung cancer. In this review, we summarize the recent advances in understanding the role of RAC1 in lung cancer and the underlying mechanisms and discuss its value in clinical therapy.