Accumulating evidence has revealed that aberrant Circular RNAs (circRNAs) expression plays important roles in carcinogenesis and tumor progression. However, their role in non-small cell lung cancer (NSCLC) remains unclear. In this study, we first used circRNA microarrays to screen for tumour-specific circRNA candidates in between NSCLC (n = 3) and adjacent lung (n = 3) tissue. Among the circRNA expression profile, two circRNAs (hsa_circ_0014130 and hsa_circ_0016760) were selected for validation in ten pairs of NSCLC and adjacent non-cancerous tissues by real-time quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Only hsa_circ_0014130 exhibited significantly overexpressed in NSCLC tissues (P < 0.001), which were further confirmed in another 36 matched tissue samples using qRT-PCR. Hsa_circ_0014130 expression significantly correlated with TNM stage (P = 0.001) and lymphatic metastasis (P = 0.004). The area under the receiver operating characteristic curve was 0.878 (95% confidence interval = 0.804–0.951; P < 0.001), which showed good diagnostic potential. Bioinformatics platforms predicted that hsa_circ_0014130 might interact with five miRNAs and their corresponding mRNAs. Gene oncology analysis and pathway analysis revealed that hsa_circ_0014130 could participate in NSCLC development. In summary, our findings indicated that hsa_circ_0014130 could be used as a potential NSCLC biomarker and might be closely related to the carcinogenesis of NSCLC.

Background: To assess the safety and efficacy of combined surgery for patients with concurrent lung cancer and severe coronary heart disease (CHD). Methods: Between 2003 and 2014, 34 patients with stage I or II lung cancer and simultaneous severe CHD underwent combined off-pump coronary artery bypass (OPCAB) grafting and lung resection. Surgically, myocardial revascularization was performed first and followed by lobectomies through the same or a second incision. Video-assisted thoracoscopes were used in some cases. Five patients also received chemotherapy before or after combined surgery in an effort to improve the long-term survival. Results: All patients survived the operation and no new myocardial infarctions (MIs) occurred in the perioperative period. The most frequent complications were cardiac arrhythmias (5 cases), atelectasis (4 cases), and pulmonary infections (2 cases). All patients were followed up for 5-60 months. Within this period, 6 patients (17.6%) died due to cancer recurrence. The 3-and 5-year survivals were 75% and 67% for these lung cancer patients, respectively. Conclusions: Combined OPCAB and pulmonary resection for early stage lung cancer patients with concurrent severe CHD is a relatively safe and effective treatment with satisfactory long-term survival rates, especially for those patients with three-vessel disease who are not usually candidates for percutaneous coronary intervention (PCI) before open surgery.

It has been documented that over-expression of metastasis-associated in colon cancer-1 (MACC1) is related to poor prognosis in non-small cell lung cancer (NSCLC). This study investigates the function and underlying molecular mechanisms of MACC1 in lung adenocarcinoma. Here, we firstly employed immunohistochemistry, western blotting, real-time PCR, and online database to demonstrate that MACC1 expression was elevated in tumor tissues compared with tumoradjacent or normal tissues. Real-time PCR, CCK-8, colony formation western blotting, Hoechst staining, and flow cytometry assays then evaluated the effects of MACC1 knockdown on the cell cycle, cell proliferation and apoptosis in A549  and H1299 adenocarcinoma cells. Result highlighted that MACC1 knockdown inhibited cell proliferation, induced G0/ G1 phase arrest and promoted cell apoptosis in vitro. Mechanistic analysis revealed it also up-regulated expression levels of bax, cleaved-caspase-3 and cleaved-PARP while down-regulating cyclin D1, c-myc, bcl-2, and β-catenin expression in A549 cells. Intriguingly, up-regulation of β-catenin suppressed G0/G1 phase arrest and apoptosis in MACC1-silenced A549 cells and this was accompanied by increased levels of cyclin D1, c-myc, and bcl-2. Collectively, our results indicate that MACC1 knockdown effectively inhibited cell proliferation and promoted apoptosis of lung adenocarcinoma cells by regulating the β-catenin pathway.