Yang Liu, Liu Guiting
Sterile Supply Center, Mudanjiang Medical College, Hongqi Hospital, Mudanjiang City 157011, Heilongjiang Province, People's Republic of China.
Department of Thoracic Surgery, Mudanjiang Medical College, Hongqi Hospital, Mudanjiang City 157011, Heilongjiang Province, People's Republic of China.
Cancer Manag Res. 2019 Apr 26;11:3565-3574. doi: 10.2147/CMAR.S194848. eCollection 2019.
As a leading cause of deaths worldwide, lung cancer is a collection of diseases with diverse etiologies which includes non-small-cell lung cancer (NSCLC). Increasing evidence reported that aberrant expression of () was involved in the tumorigenesis and progression of various malignancies. However, its role in NSCLC has not been completely clarified. In the present study, we identified the role of BANCR in the regulation of NSCLC cell viability, invasion, and apoptosis. Down-regulation of BANCR expression was significantly observed in different NSCLC cell lines (A549, H1299, H1650, H1975, SPC-A1, and PC-9), tumor tissue from NSCLC mouse model and 30 human NSCLC tissues compared with adjacent normal tissues. Overexpression of BANCR in these six NSCLC cell lines attenuated the cell viability and invasion. An increased apoptotic level caused by overexpression was also detected and displayed a conversed influence on Bcl-2 and Bax expression in mRNA and protein level. Furthermore, we identified the effect of BANCR overexpression on tumor growth in NSCLC mouse model. The restoration of expression inhibits NSCLC. Taken together, our findings shed an insight on the novel molecular mechanisms of lung NSCLC oncogenesis and provide the information for new therapeutic approaches on the disease.
作为全球主要死因之一,肺癌是一组病因多样的疾病,其中包括非小细胞肺癌(NSCLC)。越来越多的证据表明,()的异常表达与各种恶性肿瘤的发生和发展有关。然而,其在NSCLC中的作用尚未完全阐明。在本研究中,我们确定了BANCR在调节NSCLC细胞活力、侵袭和凋亡中的作用。与相邻正常组织相比,在不同的NSCLC细胞系(A549、H1299、H1650、H1975、SPC-A1和PC-9)、NSCLC小鼠模型的肿瘤组织以及30例人NSCLC组织中均显著观察到BANCR表达下调。在这六种NSCLC细胞系中过表达BANCR可减弱细胞活力和侵袭能力。还检测到过表达BANCR导致凋亡水平升高,并在mRNA和蛋白质水平上对Bcl-2和Bax表达产生相反的影响。此外,我们确定了BANCR过表达对NSCLC小鼠模型肿瘤生长的影响。BANCR表达的恢复可抑制NSCLC。综上所述,我们的研究结果揭示了NSCLC肿瘤发生的新分子机制,并为该疾病的新治疗方法提供了信息。