Survival outcomes following complete mediastinal lymphadenectomy or selective mediastinal lymphadenectomy in patients with stage I-IIIA non-small cell lung cancer: protocol for a systematic review and meta-analysis.

INTRODUCTION: Lung cancer remains the largest cause of cancer-related deaths worldwide. Surgical removal of non-small cell lung cancer (NSCLC) has the potential to achieve a cure, although there is ongoing debate regarding the significance of removing mediastinal nodes and the optimal extent of lymph node excision. The purpose of this research is to assess the survival outcomes in patients diagnosed with stage I-IIIA NSCLC who received either complete mediastinal lymphadenectomy (CML) or selective mediastinal lymphadenectomy (SML). METHODS AND ANALYSIS: The protocol follows the guidelines recommended in Preferred Reporting Items for Systematic Review and Meta-Analysis Protocols, and this meta-analysis will be conducted in accordance with the standard methodology recommended by the Cochrane Collaboration and reported in accordance with Preferred Reporting Items for Systematic Reviews and Meta-Analyses 2020 guidance. We will conduct a comprehensive search for randomised controlled trials and non-randomised studies examining the effectiveness of CML compared with SML in patients with stage I-IIIA NSCLC. Two authors will perform a comprehensive search of the MEDLINE/PubMed, Embase, the Cochrane Library, CNKI, WanFang, Sinomed, VIP and Web of Science databases. There will be no restrictions on language or publication date, and the search will be conducted on 10 April 2024, with ongoing searches for new research. Reference lists will also be checked and pertinent journals will be hand searched. The primary outcomes include overall survival (OS) and disease-free survival (DFS), while the secondary outcomes consist of 1-year, 3-year and 5-year OS rates and 1-year, 3-year and 5-year DFS rates. Two independent reviewers will screen, extract data, assess quality and evaluate the potential for bias in the selected research, with a third acting as arbitrator. Subgroup analyses and sensitivity analyses are planned. The quality of the evidence will be evaluated using Grading of Recommendations Assessment, Development and Evaluation. Review Manager V.5.4 will be used for the analysis and synthesis process. ETHICS AND DISSEMINATION: Ethical review and approval are not necessary for this study because it is based on a secondary analysis of the literature. The results will be submitted for reporting in a peer-reviewed publication. STUDY REGISTRATION: Open Science Framework (https://doi.org/10.17605/OSF.IO/PN7UQ).

CircCDK17 promotes the proliferation and metastasis of ovarian cancer cells by sponging miR-22-3p to regulate CD147 expression.

Ovarian cancer (OC) is a common malignancy in women of reproductive age. Circular RNAs (circRNAs) are emerging players in OC progression. We investigated the function and mechanism of circular RNA hsa_circ_0027803 (circCDK17) in OC pathogenesis. Real­time PCR (RT-qPCR) and western blot were utilized for gene and protein expression analysis, respectively. Cell counting kit­8 (CCK-8), EdU and Transwell assays investigated OC cell proliferation, migration and invasion. The associations between circCDK17, miR-22-3p and CD147 were examined by dual-luciferase reporter and RNA-protein immunoprecipitation (RIP) assays. The in vivo model of OC nude mice was constructed to explore the role of circCDK17. CircCDK17 was increased in OC tissue and cells, and patients with higher expression of circCDK17 had a shorter survival. CircCDK17 downregulation inhibited OC cell proliferation, migration and invasion, and reduced epithelial-mesenchymal transition (EMT)-related markers. In vivo experiments showed that circCDK17 silencing inhibited OC tumor growth and metastasis. CircCDK17 depletion reduced CD147 level via sponging miR-22-3p. MiR-22-3p knockdown overturned effect of circCDK17 depletion on OC cell proliferation, migration and invasion. Meanwhile, overexpressed CD147 restored functions of circCDK17 downregulation on OC development. CircCDK17 is an important molecule that regulates OC pathogenic process through miR-22-3p/CD147.