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Abstract. Lung cancer is the most frequently diagnosed cancer and the leading cause of cancer-related mortality worldwide. In the present study, we focused on LIM and SH3 protein 1 (LASP-1), a key molecule involved in the development of multiple cancers, and attempted to elucidate its effect on the oncogenesis of lung cancer. We determined the expression level of LASP-1 in lung cancer using reverse transcription-quantitative polymerase chain reaction and western blot analysis, and also studied the potential function of LASP-1 in lung cancer cell growth, apoptosis and migration by small interfering RNA transfection. The results revealed that the levels of LASP-1 mRNA and protein were abnormally high in lung cancer cells. Following RNA interference of LASP-1, the proliferation and migration ability of the human cancer cell line A549 were significantly decreased. In addition, fluorescence-activated cell sorting analysis indicated that the apoptotic process in the A549 cell line was induced by the silencing of LASP-1. Our study is the first to investigate the potential of LASP-1 in lung cancer, and revealed its significant role in regulating the growth and metastasis of lung cancer cells. The present study suggests that LASP-1 has potential as a therapeutic target in the treatment of lung cancer in the clinic. IntroductionLung cancer is the most frequently diagnosed cancer and the leading cause of cancer-related mortality worldwide in both males and females (1), accounting for more than 1.4 million mortalities per year. Moreover, with the high and increasing number of smokers in a number of Asian and developing countries, it is anticipated that the incidence of lung cancer will continue to increase over the next decades. The rates of lung cancer are mainly determined by smoking patterns, although other factors, including medical, occupational and environmental radiation exposure, have also been demonstrated to increase the risk of lung cancer (2).Lung cancer is a heterogeneous disease that has historically been divided into two main types based on the disease patterns and treatment strategies: small cell-lung cancer (SCLC) and non-small cell-lung cancer (NSCLC) (3,4). The expressions of various oncogenes have been investigated in NSCLC and SCLC. The complex multiple genetic lesions in lung cancer are composed of two major forms (5): mutations activating the dominant cellular proto-oncogenes, and as those inactivating the tumor suppressor genes. The activation of RAS, MYC and HER-2/NEU genes is usually associated with an adverse prognosis of lung cancer (6-8), while the overexpression of tumor suppressor genes including VHL, RB and p53 demonstrate a positive outcome in the recovery of lung cancer patients (2).Chemotherapy remains the cornerstone of treatment for limited-and extensive-stage lung cancer. Surgery is also considered for certain stages (9). However, these traditional treatments only provide a modest benefit with considerable toxicity for advanced lung cancer (10). There is an urgent requirement to develop...

We previously found a panel of autoantibodies against multiple tumor-associated antigens (BMI-1, HSP70, MMP-7, NY-ESO-1, p53 and PRDX6) that might facilitate early detection of esophagogastric junction adenocarcinoma and esophageal squamous cell carcinoma. Here we aimed at assessing the diagnostic performance of these autoantibodies in breast cancer patients. Enzyme-linked immunosorbent assay was applied to detect sera autoantibodies in 123 breast cancer patients and 123 age-matched normal controls. We adopted logistic regression analysis to identify optimized autoantibody biomarkers for diagnosis and receiver-operating characteristics to analyze diagnostic efficiency. Five of six autoantibodies, BMI-1, HSP70, NY-ESO-1, p53 and PRDX6 demonstrated significantly elevated serum levels in breast cancer compared to normal controls. An optimized panel composed of autoantibodies to BMI-1, HSP70, NY-ESO-1 and p53 showed an area under the curve (AUC) of 0.819 (95% CI 0.766-0.873), 63.4% sensitivity and 90.2% specificity for diagnosing breast cancer. Moreover, this autoantibody panel could differentiate patients with early stage breast cancer from normal controls, with AUC of 0.805 (95% CI 0.743-0.886), 59.6% sensitivity and 90.2% specificity. Our findings indicated that the panel of autoantibodies to BMI-1, HSP70, NY-ESO-1 and p53 as serum biomarkers have the potential to help detect early stage breast cancer.