Background: The overall survival (OS) in non-small cell lung cancer (NSCLC) is poor, with median OS of advanced NSCLC with standard systemic chemotherapy being reported at 13.6 months and the 5-year survival rate at less than 15%. Therefore, the aim of this study was to evaluate Endostar combined with chemotherapy in patients with advanced NSCLC. Methods: Data on 116 cases of pathologically confirmed stage IIIB-IV NSCLC were retrospectively collected. The control group was treated with chemotherapy combined with intravenous infusion of Endostar while the test group received durative transfusion of Endostar. The short-term therapeutic effects including overall response rate (ORR), disease control rate (DCR), and safety were evaluated in both groups. In the follow-up, progression-free survival (PFS) and OS were also analysed. Results: In the test group, the ORR was 53.4%, which was similar to that in the control group (44.8%) (p > 0.05). However, the DCR in the test group (86.2%) was significantly higher than that in the control group (70.7%) (p < 0.01). The median time to progression in the test group (6 months) was also significantly longer than that in the control group (4 months). Importantly, the median OS in the test group (17.5 months) was improved compared to the control group (13.5 months). The 1-year survival rate in the test and control groups was 9.7 and 15.8%, respectively. There was no significant difference in side effects (including thrombocytopenia, leucopenia, nausea, and vomiting) between the two groups. Conclusions: Endostar durative transfusion combined with chemotherapy showed a higher DCR, longer PFS and OS time, and was well tolerated in patients with advanced NSCLC.
Tyrosine kinase inhibitors (TKIs) bring significant benefits for patients with cancers harboring epidermal growth factor receptor (EGFR) mutations. However, after treatment for a certain period, most patients ultimately acquire resistance. Numerous studies indicated that PI3K has an important role in tumor cell growth and drug sensitivity. Furthermore, inhibition of PI3K may lead to sensitization of non-small cell lung cancer (NSCLC) cells to EGFR-TKIs. The aim of the present study was to explore whether LY294002, an inhibitor of PI3K, is able to improve the sensitivity of NSCLC cell lines with wild-type EGFR to the EGFR-TKI erlotinib. An MTT assay was used to examine the effect of combined treatment with LY294002 and erlotinib on cell survival of two EGFR wild-type NSCLC cell lines, NCI-H661 and NCI-H460. Furthermore, flow cytometry was used to assess apoptosis in NCI-H661 and NCI-H460 cells after treatment with erlotinib and LY294002. In addition, the expression of downstream proteins was detected by western blot analysis. The results indicated that the number of viable NCI-H661 and NCI-H460 cells was dose-dependently reduced by erlotinib or LY294002. Compared to treatment with erlotinib alone, the cell apoptosis was enhanced if combined treatment of erlotinib and LY294002 was performed in NCI-H661 cells. Furthermore, combination treatment of erlotinib and LY294002 resulted in a significant reduction of phosphorylated p70S6K levels in NCI-H661 [PI3K catalytic subunit alpha (PI3KCA) wild-type] cells. However, this phenomenon was not observed in the NCI-H460 cell line (PIK3CA mutant-type). In conclusion, the present study indicated that inhibition of PI3K may have the potential to improve the sensitivity of NSCLC cells to an EGFR-TKI. However, the therapeutic effect may depend on the mutation status of PIK3CA.
Background: There is increasing evidence that long non-coding RNA (lncRNA) small nucleolar RNA host gene 20 (SNHG20) plays an important role in cancer. However, the function of SNHG20 in lung adenocarcinoma is unclear. The aim of our study was to investigate the roles of SNHG20 in lung adenocarcinoma. Methods: Real-time quantitative polymerasechain reaction (RT-qPCR) was used to calculate the expression of SNHG20, miR-342 and DEAD-box helicase 49 (DDX49). Dual luciferase reporter gene assay was applied to verify whether miR-342 binding to SNHG20 and DDX49. The expression correlation between miR-342 and SNHG20 or DDX49 was assessed using Pearson's correlation analysis. Results: SNHG20 and DDX49 were overexpressed, while miR-342 was lowly expressed in lung adenocarcinoma tissues and cell lines. Knockdown of SNHG20 suppressed cell proliferation, invasion and enhanced cell apoptosis. SNHG20 was found to directly bind to miR-342 and regulate the expression of miR-342. MiR-342 directly targeted DDX49 and the expression of miR-342 had negative connection with DDX49 in lung adenocarcinoma tissues. Knockdown of DDX49 inhibited the progression of lung adenocarcinoma. DDX49 partially restored the functions of SNHG20 in A549 cells. Conclusions: SNHG20 regulated lung adenocarcinoma cell proliferation, invasion and promoted cell apoptosis via miR-342/DDX49 axis. Our findings demonstrate that SNHG20/miR-342/DDX49 axis plays an important role in lung adenocarcinoma, providing a novel insight into the treatment of lung adenocarcinoma.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.