Background: Uni-portal video-assisted thoracoscopic surgery (VATS) has become a popular type of thoracic surgery. However, improvements to the closure of the single drainage tube hole are still in need.Methods: From February 2019 to May 2019, we included 50 patients who received uni-portal VATS for lung disease or mediastinal disease and simple continuous suture to strengthen the closure of intramuscle combined with removal-free stitches on the skin. Follow-up items included incision length, chest tube drainage amount, chest tube drainage time, incision effusion leakage, postoperative subcutaneous emphysema, postoperative pain score.Results: A total of 50 patients were included in this study, including 23 males and 27 females, with an average age of 60.08±9.73 years old. The mean drainage on the first day after operation was 236.56±141.50 mL, while the mean pain score on the first day after operation was 4.16±1.70. Among 50 patients, only two cases of subcutaneous emphysema occurred.Conclusions: Applying innovative simple continuous suture to strengthen the closure of intra-muscle combined with removal-free stitches on the skin into the closure of uni-portal VATS is safe and feasible.

In view of the important roles played by Kinetochore proteins in mitosis, we believed that they may contribute to the development and progression of human cancers, which has been reported recently elsewhere. Kinetochore-associated 1 (KNTC1) participates in the segregation of sister chromatids during mitosis, the effects of which on non-small-cell lung cancer (NSCLC) remain unclear. Here, we sought to identify the biological significance of KNTC1 in NSCLC. KNTC1 protein expression in NSCLC tissues was investigated by immunohistochemistry. Lentivirus delivered short hairpin RNA (shRNA) was utilized to establish KNTC1 silence NSCLC cell lines. The effects of KNTC1 depletion on NSCLC cell proliferation, migration, apoptosis, and tumor formation were analyzed by MTT assay, wound-healing assay, transwell assay, flow cytometry assay, and in nude mouse models in vivo. After KNTC1 reduction, NSCLC cell viability, proliferation, migration, and invasion were restrained. A xenograft tumor model was also provided to demonstrate the inhibited tumorigenesis in NSCLC. In addition, the downstream mechanism analysis indicated that KNTC1 depletion was positively associated with PSMB8. The findings of the present study suggested that KNTC1 may have a pivotal role in mediating NSCLC progression and may act as a novel therapeutic target for NSCLC.