A learning curve for VATS lobectomy existed in this series. The surgeon became more proficient after 30-60 cases and was able to perform the procedure with decreased blood loss and operative time.

Long noncoding RNA, long intergenic non-protein-coding RNA p53-induced transcript (LINC-PINT) was showed to be involved in cancer development. However, the biological effect of LINC-PINT on nonsmall cell lung cancer (NSCLC) remains unknown. Here, we aimed to investigate the role and underlying mechanism of LINC-PINT in NSCLC. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to measure the level of LINC-PINT in NSCLC tissues and cell lines. Cell counting kit-8 (CCK-8), flow cytometry, migration and transwell invasion assays were used to investigate cell proliferation, cell cycle, cell migration and invasion, respectively. The targets of LINC-PINT were verified by both luciferase reporter assay and RNA immunoprecipitation assay. Tumour xenografts were used to reveal the effect of LINC-PINT on tumourigenesis in vivo. We observed that LINC-PINT expression increased in both NSCLC tissues and cell lines. Function assays exhibited that LINC-PINT reduced NSCLC cell proliferation, cell cycle, cell migration and invasion in vitro. We also indicated that LINC-PINT mediated inhibitory effect on cell proliferation, cell cycle, cell migration and invasion by miR-208a-3p/programmed cell death 4 (PDCD4) in NSCLC cells. These findings indicated that LINC-PINT functions as a tumour-suppressor that exerts important regulatory roles in NSCLC progression by sponging miR-208a-3p/PDCD4.

Non-small cell lung cancer (NSCLC) is a common malignant tumor. Although the abnormal expression and potential clinical prognostic value of histone deacetylase 1 (HDAC1) were recently discovered in many kinds of cancer, the roles and molecular mechanisms of HDAC1 in NSCLC is still limited. The CCK-8 assay is used to evaluate the viability of NSCLC cells. Downregulation of HDAC1 by shRNA. The TUNEL assay was used to evaluate the role of HDAC1 in NSCLC apoptosis. To evaluate the role of HDAC1 in NSCLC cells migration, the Boyden chamber transwell assay and wound healing assay were used. To evaluate the cells invasion, the matrigel precoated Transwell assay was used. Enzyme-linked immunosorbent assays (ELISAs) were used to detect the level of vascular endothelial growth factor (VEGF) and IL-8 in NSCLC. To investigate the role of HDAC1 in angiogenesis, the tube formation assay was investigated. In this study, we showed that HDAC1 expression was elevated in NSCLC lines compared to that in normal liver cells LO2. Furthermore, downregulation of HDAC1 inhibited cell proliferation, prevented cell migration, decreased cell invasion, reduced tumor angiogenesis and induced cell apoptosis. In summary, HDAC1 may be regarded as a potential indicator for NSCLC patient treatment.