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Lung cancer is among the leading causes of cancer-associated mortality worldwide, with a low 5-year survival rate of 16.1%. However, the underlying molecular mechanisms behind lung cancer tumorigenesis remain largely unknown. Long non-coding RNAs (lncRNAs) have been demonstrated to serve a function in the tumorigenesis of multiple types of cancer. The objective of the present study was to identify the function of a newly identified lncRNA zinc finger E-box-binding homeobox 2 antisense RNA 1 (ZEB2-AS1) in human lung cancer. Results demonstrated that the transcript level of ZEB2-AS1 in human lung cancer was markedly upregulated in vivo and in vitro. The knockdown of ZEB2-AS1 in A549 and NCI-H292 cells, and the overexpression of ZEB2-AS1 in H-125 and H1975 cells, altered colony formation and cell proliferative rate, as examined using colony formation and cell proliferation assays. Western blot analysis revealed that the knockdown of ZEB2-AS1 in A549 and NCI-H292 cells increased the protein levels of B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), caspase-3 and - 9, upregulated the relative activities of caspase-3 and -9, and had no observable effect on caspase-8 activity. Similarly, the overexpression of ZEB2-AS1 in H-125 and H1975 cells resulted in decreased expression of caspase-3, caspase-9, Bcl-2 and Bax. The results identified the effects of lncRNA ZEB2-AS1 on lung cancer progression through promoting its proliferation and inhibiting cell apoptosis, indicating that ZEB2-AS1 may serve as a novel prognostic factor for the diagnosis and treatment of human lung cancer in the clinic. [ABSTRACT FROM AUTHOR]

Background: Basic fibroblast growth factor (bFGF) is known to stimulate angiogenesis and thus to influence the proliferation, migration and survival of tumor cells. Many studies examined the relationship between human bFGF overexpression and survival in lung cancer patients, but the results have been mixed. To systematically summarize the clinical prognostic function of bFGF in lung cancer, we performed this systematic review with meta-analysis. Method: Studies were identified by an electronic search of PubMed, EMBASE, China National Knowledge Infrastructure and Wanfang databases, including publications prior toAugust 2014. Pooled hazard ratios (HR) for overall survival (OS) were aggregated and quantitatively analyzed by meta-analysis. Results: Twenty-two studies (n = 2154) were evaluated in the meta-analysis. Combined HR suggested that bFGF overexpression had an adverse impact on survival of patients with lung cancer(HR = 1.202,95%CI, 1.022–1.382). Our subgroup analysis revealed that the combined HR evaluating bFGF expression on OS in operable non-small cell lung cancer (NSCLC) was 1.553 (95%CI, 1.120–1.986); the combined HR in small cell lung cancer (SCLC) was 1.667 (95%CI, 1.035–2.299). There was no significant impact of bFGF expression on survival in advanced NSCLC. Conclusion: This meta-analysis showed that bFGF overexpression is a potential indicator of worse prognosis for patients with operable NSCLC and SCLC, but is not associated with outcome in advanced NSCLC. The data suggests that high bFGF expression is highly related to poor prognosis. Nevertheless,more high-quality studies should be performed in order to provide additional evidence for the prognostic value of bFGF in lung cancer. [ABSTRACT FROM AUTHOR]

Lung cancer is currently the leading cause of cancer-related death in worldwide, non-small cell lung cancer (NSCLC) accounts for about 85% of all lung cancers. Surgery, platinum-based chemotherapy, molecular targeted agents and radiotherapy are the main treatment of NSCLC. With the strategies of treatment constantly improving, the prognosis of NSCLC patients is not as good as before, new sort of treatments are needed to be exploited. Programmed death 1 (PD-1) and its ligand PD-L1 play a key role in tumor immune escape and the formation of tumor microenvironment, closely related with tumor generation and development. Blockading the PD-1/PD-L1 pathway could reverse the tumor microenvironment and enhance the endogenous antitumor immune responses. Utilizing the PD-1 and/or PD-L1 inhibitors has shown benefits in clinical trials of NSCLC. In this review, we discuss the basic principle of PD-1/PD-L1 pathway and its role in the tumorigenesis and development of NSCLC. The clinical development of PD-1/PD-L1 pathway inhibitors and the main problems in the present studies and the research direction in the future will also be discussed. [ABSTRACT FROM AUTHOR]