Uniportal video-assisted anatomical segmentectomy: an analysis of the learning curve.

BACKGROUND: This study aimed to demonstrate the learning curve of anatomical segmentectomy performed by uniportal video-assisted thoracoscopic surgery (U-VATS). METHOD: We conducted a retrospective study of U-VATS segmentectomies performed by the same surgeon between September 2019 and August 2022. The learning curve was demonstrated using risk-adjusted cumulative sum (RA-CUSUM) analysis in terms of perioperative complications, which reflected surgical quality and technique proficiency. The surgical outcomes were also compared between different phases. RESULT: The complication-based learning curve of U-VATS segmentectomy could be divided into two phases based on RA-CUSUM analysis: phase I, the initial learning phase (cases 1-50) and phase II, the proficiency phase (cases 51-141). Significantly higher complication rates (24.0 vs. 8.8%, p=0.013), longer surgical times (119.8±31.9 vs. 106.2±23.8 min, p=0.005), and more blood loss (20 [IQR, 20-30] vs. 20 [IQR, 10-20] ml, p=0.003) were observed in phase I than in phase II. CONCLUSION: The learning curve of U-VATS segmentectomy consists of two phases, and at least 50 cases were required to gain technique proficiency and achieve high-quality surgical outcomes.

E2F1-activated LINC01224 drives esophageal squamous cell carcinoma cell malignant behaviors via targeting miR-6884-5p/DVL3 axis and activating Wnt/ß-catenin signaling pathway.

Current evidence has unveiled that long non-coding RNAs (lncRNAs) are pivotal regulators in the development of cancers. This study aimed to investigate the potential mechanisms of LINC01224 in esophageal squamous cell carcinoma (ESCC) cells. RT-qPCR analysis was done to test LINC01224 expression in ESCC cells. Functional assays were conducted to assess the influences of LINC01224 on ESCC cell functions. Mechanism assays were carried out to detect the regulatory mechanisms of LINC01224 at post-transcriptional and transcriptional levels. Briefly, LINC01224 expression was remarkably high in ESCC cells. LINC01224 silence restricted the proliferative, migratory, and invasive capabilities of ESCC cells. Moreover, LINC01224 could combine with miR-6884-5p by acting as a ceRNA. Further, DVL3 was proved to be targeted by miR-6884-5p. Importantly, LINC01224 could switch on Wnt/ß-catenin signaling pathway by via enhancing DVL3 expression. Additionally, E2F1 could serve as a transcription factor to stimulate LINC01224 transcription. In summary, our study elucidated that E2F1-activated LINC01224 regulated miR-6884-5p/DVL3 to actuate the Wnt/ß-catenin signaling pathway, which facilitates multiple phenotype of ESCC cells, including proliferation, migration, and invasion. Our findings might offer potential therapeutic targets for ESCC treatment.