Systematic review and meta-analysis on perioperative intervention to prevent postoperative atelectasis complications after thoracic surgery.

BACKGROUND: In clinical general thoracic surgery, the prevalence of atelectasis is relatively high. Perioperative interventions can affect the probability of patients with atelectasis after surgery. Therefore, the incidence of perioperative intervention to prevent atelectasis after thoracic surgery was discussed using meta-analysis in this study. METHODS: The articles were searched in the English database PubMed and Chinese databases including China National Knowledge Infrastructure (CNKI), VIP, and China Journal Full-text Database (CJFD). The duration for publication time of the articles was from the database inception to March 2021, and the articles were required to be randomized controlled trials (RCTs) using interventions [such as changing the dose of general anesthesia, continuous positive end expiratory pressure (PEEP), non-invasive pressure support ventilation, and physical therapy] after thoracic surgery (such as pulmonary lobectomy, sternum surgery, and lung cancer surgery) for the treatment of atelectasis. The software RevMan 5.3 provided by the Cochrane Collaboration was used for meta-analysis. RESULTS: A total of 5 articles were obtained, including 375 cases in the control group and 268 cases in the intervention treatment group. A meta-analysis was performed on the included articles, combined effect model analysis results showed that compared with the control group, the use of PEEP during mechanical ventilation can significantly reduce the incidence of atelectasis [odds ratio (OR) =0.46; 95% confidence interval (CI): 0.31-0.67; Z=3.94; P<0.0001]. DISCUSSION: Perioperative intervention was more effective for postoperative atelectasis and other complications.

CircRNA CDR1as/miR-641/HOXA9 pathway regulated stemness contributes to cisplatin resistance in non-small cell lung cancer (NSCLC).

BACKGROUND: Cisplatin (DDP) is the first-line chemotherapeutic drug for non-small cell lung cancer (NSCLC), and long-term DDP stimulation increased resistance of NSCLC cells to this drug by enriching cancer stem cells (CSCs), which contributed to recurrence and worse prognosis of NSCLC, but the molecular mechanisms are still not fully delineated. METHODS: Real-Time qPCR and Western Blot analysis were conducted to examine gene expressions at mRNA and protein levels, respectively. Dual-luciferase reporter gene system was used to validate the targeting sites among circRNA CDR1as, miR-641 and HOXA9 mRNA. Cell growth was evaluated by CCK-8 assay, trypan blue staining assay and colony formation assay. The Annexin V-FITC/PI double staining method was employed to measure cell apoptosis ratio. Spheroid formation and flow cytometer assay was used to evaluate cell stemness. Xenograft mice models were established to measure tumorgenicity in vivo, and Ki67 expressions in mice tumor tissues were examined by immunohistochemistry (IHC). RESULTS: Here we identified a novel circRNA CDR1as/miR-641/Homeobox protein Hox-A9 (HOXA9) pathway regulated stemness and DDP chemoresistance in NSCLC. Mechanistically, circRNA CDR1as and HOXA9 were high-expressed, while miR-641 was low-expressed in DDP-resistant NSCLC cells, instead of their corresponding parental DDP-sensitive NSCLC cells. Additionally, we validated that circRNA CDR1as positively regulated HOXA9 in NSCLC cells by serving as an RNA sponge for miR-641, and knock-down of circRNA CDR1as increased the sensitivity of DDP-resistant NSCLC cells, which were reversed by downregulating miR-641 and upregulating HOXA9. Consistently, overexpression of circRNA CDR1as increased drug resistance of DDP-sensitive NSCLC cells by regulating miR-641/HOXA9 axis. In addition, the expression levels of stemness signatures (SOX2, OCT4 and Nanog) were higher in DDP-resistant NSCLC cells, which also tended to form spheres and enrich CD44+CD166+ population compared to their parental DDP-sensitive NSCLC cells, suggesting that CSCs were enriched in DDP-resistant NSCLC cells. Notably, knock-down of circRNA CDR1as inhibited stemness of DDP-resistant NSCLC cells by inhibiting HOXA9 through upregulating miR-641. CONCLUSIONS: Taken together, this study identified that circRNA CDR1as regulated stemness and DDP chemoresistance in NSCLC cells by targeting miR-641/HOXA9 axis.

MiR-625 Inhibits Tumor Cell Invasion, Migration and EMT by Negatively Regulating the Expression of Resistin in Non-Small Cell Lung.

PURPOSE: To investigate the role of miR-625 on the invasion, migration, and epithelial-mesenchymal transition (EMT) of non-small cell lung carcinoma (NSCLC) cells, and the related mechanisms. MATERIALS AND METHODS: The expression levels of miR-625 and Resistin mRNA in 80 pairs of NSCLC and para-cancerous lung tissues were analyzed by RT-PCR. The relationship between miR-625 and Resistin was predicted by bioinformatics and verified by a dual-luciferase gene reporter assay. NSCLC cells were transfected with Resistin plasmids, si-Resistin plasmids, miR-625 mimics, or miR-625 inhibitors, and proliferation, invasion, and migration were determined by CCK-8, Transwell, and wound scratch assays, respectively. EMT-related proteins were determined by Western blot assay. A xenograft model of NSCLC was established in nude mice to validate the in vitro findings. RESULTS: MiR-625 was significantly downregulated in NSCLC tissue compared to paired para-cancerous lung tissues, while Resistin was markedly increased in tumor tissue. The expression levels of miR-625 and Resistin were negatively correlated in NSCLC tissues, and high levels of Resistin correlated with greater tumor differentiation, more advanced clinical staging, and lymph node metastasis. Furthermore, Resistin was a target gene of miR-625, and the latter downregulated Resistin to inhibit the EMT, proliferation, invasion, and migration of NSCLC cells in vitro, likely via the PI3K/AKT/Snail signaling pathway. Finally, miR-625 also inhibited the tumorigenic effect of NSCLC cells in vivo by downregulating Resistin. CONCLUSION: MiR-625 acts as a tumor suppressor in NSCLC and inhibits tumor cell invasion and metastasis by blocking the Resistin/PI3K/AKT/Snail pathway and by decreasing EMT.

Loss of phosphatase and tensin homolog expression correlates with clinicopathological features of non-small cell lung cancer patients and its impact on survival: A systematic review and meta-analysis.

BACKGROUND: Phosphatase and tensin homolog ( PTEN ), regarded as a tumor suppressor gene, may act as a prognostic biomarker in human cancers. METHODS: All eligible studies from MEDLINE, Embase, CENTRAL, and the Chinese BioMedical Literature Database to October 2016 were incorporated. Two reviewers independently screened the literature according to inclusion and exclusion criteria, extracted the data, assessed the methodological quality of the included studies, and conducted meta-analysis. RESULTS: A total of 2486 patients from 19 studies were included. PTEN expression was significantly correlated with gender, smoking history, histology (adenocarcinoma [ADC] vs. squamous cell carcinoma), tumor node metastasis stage (I-II vs. III-IV), N status (N0 vs. N1-N3), and distant metastasis (M0 vs. M1). Loss of PTEN expression was associated with poorer overall survival, but had no significant association with disease-free survival. Subgroup analysis showed that negative PTEN expression was associated with a poorer outcome in Asian and ADC patients, but not in Western or squamous cell carcinoma patients. CONCLUSION: Loss of PTEN might play an unfavorable prognostic role for overall survival of non-small cell lung cancer patients, especially Asian or ADC patients.