Efficacy and safety of early chest tube removal after selective pulmonary resection with high-output drainage: A systematic review and meta-analysis.

BACKGROUND: There is controversy over the drainage threshold for removal of chest tubes in the absence of significant air leakage after selective pulmonary resection. METHODS: A comprehensive search of online databases (PubMed, Web of Science, Embase, Cochrane Library, Scopus, Ovid, Elsevier, Ebsco, and Wiley) and clinical trial registries (WHO-ICTRP and ClinicalTrials.gov) was performed to investigate the efficacy and safety of early chest tube removal with high-output drainage. Primary outcome (postoperative hospital day) and secondary outcomes (30-day complications, rate of thoracentesis, and chest tube placement) were extracted and synthesized. Subgroup analysis, meta-regression, and sensitivity analysis were used to explore the potential heterogeneity. Study quality was assessed with the Newcastle-Ottawa Scale, and evidence was graded using the Grading of Recommendations Assessment, Development and Evaluation (GRADE) assessment by the online GRADEpro Guideline Development Tool. RESULTS: Six cohort studies with a total of 1262 patients were included in the final analysis. The postoperative hospital stay in the high-output group was significantly shorter than in the conventional treatment group (weighted mean difference: -1.34 [-2.34 to -0.34] day, P = .009). While there was no significant difference between 2 groups in 30-day complications (relative ratio [RR]: 0.92 [0.77-1.11], P = .38), the rate of thoracentesis (RR: 1.93 [0.63-5.88], P = .25) and the rate of chest tube placement (RR: 1.00 [0.37-2.70], P = .99). According to the sensitivity analysis, the relative impacts of the 2 groups had already stabilized. Subgroup analysis revealed that postoperative hospital stay was modified by Newcastle-Ottawa Scale score. The online GRADEpro Guideline Development Tool presented very low quality of evidence for the available data. CONCLUSIONS: This meta-analysis revealed that it is feasible and safe to remove a chest tube with high-output drainage after pulmonary resection for selected patients.

LncRNA LINC00511 promotes COL1A1-mediated proliferation and metastasis by sponging miR-126-5p/miR-218-5p in lung adenocarcinoma.

BACKGROUND: Lung adenocarcinoma (LUAD) is currently the leading cause of cancer-related death worldwide. Long noncoding RNAs (lncRNAs) play key roles in tumor occurrence and development as crucial cancer regulators. The present study aimed to explore the molecular mechanism and regulatory network of Linc00511 in LUAD and to identify new potential therapeutic targets for LUAD. METHODS: Real-time quantitative polymerase chain reaction (RT-qPCR) was performed to determine the relative Linc00511 levels in LUAD tissues and cells. The proliferation, apoptosis, migration, and invasion abilities of LUAD cells were assessed by a Cell Counting Kit-8 (CCK-8) assay, a colony formation assay, flow cytometry, and a Transwell assay. Changes in hsa_miR-126-5p, hsa_miR-218-5p, and COL1A1 expression were analyzed using western blotting and RT-qPCR. Targeted binding between miR-126-5p/miR-218-5p and Linc00511 or COL1A1 was verified with a luciferase reporter system and confirmed by an RNA pulldown assay. The participation of the PI3K/AKT signaling pathway was confirmed via western blotting. Xenograft animal experiments were performed to detect the impact of Linc00511 on LUAD tumor growth in vivo. RESULTS: In the present work, we observed that Linc00511 was upregulated in LUAD tissues and cells. Loss/gain-of-function experiments indicated that knockdown of Linc00511 significantly inhibited LUAD cell proliferation, migration and invasion and promoted LUAD cell apoptosis, whereas overexpression of Linc00511 showed the opposite effects. In addition, we determined that Linc00511 promoted COL1A1-mediated cell proliferation and cell motility by sponging miR-126-5p and miR-218-5p. Moreover, Linc00511 activated the PI3K/AKT signaling pathway through upregulation of COL1A1. Finally, silencing of Linc00511 inhibited LUAD tumor growth in vivo. CONCLUSIONS: Linc00511 acts as a competing endogenous RNA to regulate COL1A1 by targeting miR-126-5p and miR-218-5p, thereby promoting the proliferation and invasion of LUAD cells.