The feasibility and safety of simultaneous bilateral video-assisted thoracic surgery for the treatment of bilateral pulmonary lesions.

Background: The aim of this study was to evaluate the feasibility and safety of simultaneous bilateral video-assisted thoracic surgery (VATS) for the treatment of bilateral pulmonary lesions. Methods: The data of 11 patients who received simultaneous bilateral pulmonary surgery using VATS in the Department of Thoracic Surgery of The Third Affiliated Hospital of Naval Medical University between January 2016 and August 2021 were retrospectively analyzed. Results: The cases of four male and seven female patients, with a mean age of 57.54 ± 8.37 years (range, 44-67 years), were reviewed. Nonanatomic wedge resection, pulmonary segmentectomy or lobectomy via VATS were performed depending on each patient's situation. Mean 1 second forced expiratory volume (FEV1) was 2.55 ± 0.66 L(range, 1.49-3.88 L), mean intraoperative bleeding volume was 91.81 ± 49.56 mL(range, 30-150 mL), mean operating time was 273.72 ± 68.98 min(range, 132-390 min), and mean drainage duration was 5.27 ± 3.60 days(range, 2-14 days), with a mean total drainage volume of 1,515.90 ± 772.75 mL(range, 530-3,225 mL). Only one postoperative complication (air leakage) occurred, with an overall complication rate of 9.09%. The mean postoperative hospital stay was 8.81 ± 3.60 days (range, 5-18 days), and the mean total cost of hospitalization was 67,054.53 ± 20,896.49 RMB (range, 47,578.45-123,530.8 RMB). Conclusions: Simultaneous bilateral pulmonary surgery using VATS for the treatment of bilateral pulmonary lesions is safe and feasible and can therefore be considered after strict preoperative evaluation of the patient.

An original design of remote robot-assisted intubation system.

The success rate of pre-hospital endotracheal intubation (ETI) by paramedics is lower than physicians. We aimed to establish a remote robot-assisted intubation system (RRAIS) and expected it to improve success rate of pre-hospital ETI. To test the robot's feasibility, 20 pigs were intubated by direct laryngoscope or the robot system. Intubation time, success rate, airway complications were recorded during the experiment. The animal experiment showed that participants achieved a higher success rate in absolute numbers by the robot system. In summary, we have successfully developed a remote robot-assisted intubation system. It is promising for RRAIS to improve the success rate of pre-hospital ETI and change the current rescue model.

MicroRNA-92a promotes epithelial-mesenchymal transition through activation of PTEN/PI3K/AKT signaling pathway in non-small cell lung cancer metastasis.

MicroRNAs (miRNAs) have important roles in various cancers, including non-small cell lung cancer (NSCLC). Although several miRNAs have reported to be involved in the development of NSCLC, understanding the regulatory roles of other miRNAs in NSCLC is essential. Therefore, the aim of the current study was to explore the roles and mechanisms of screened miRNAs in NSCLC. First, the differentially expressed miRNAs that were screened based on GSE29248 microarray data retrieved from Gene Expression Omnibus (GEO). The expression of miR-92a, acted as an oncogene in many cancers, was validated using quantitative real-time PCR (qRT-PCR), and then its association with overall survival was analyzed. The efficacy of miR-92a to promote cell proliferation, invasion and metastasis was evaluated in vitro, and in vivo. Then, the role of miR-92a in epithelial-mesenchymal transition (EMT), a key step of the progression of tumor cell metastasis, was investigated in NSCLC cells. The association of miR-92a and its downstream target was investigated in both cell line and clinical specimens. Furthermore, gain- and loss-of-function studies of the phosphatase and tensin homolog (PTEN) were performed to assess whether the effect of miR-92a promoted growth and metastasis of NSCLC cells were via targeting PTEN. Our results showed that miR-92a was significantly upregulated in NSCLC tissues and NSCLC cell lines, and was positively associated with poor prognosis of NSCLC patients. The overexpression of miR-92a enhanced EMT-relatived protein levels, promoted NSCLC cell migration and invasion in vitro, and increased tumor growth in vivo. Bioinformatic prediction and function assay suggested that PTEN, a negative regulator of PI3K/AKT pathway, was a direct target of miR-92a. It was found that PTEN expression was inversely correlated with miR-92a in NSCLC tissues. In addition, miR-92a could activate the PI3K/AKT pathway by inhibiting PTEN expression. Notably, Transwell and wound healing assays demonstrated that altering PTEN expression abrogated the promotive effects of miR-92a on NSCLC cell migration and invasion. Taken together, these results demonstrated that miR-92a induced EMT and regulated cell migration and invasion in the NSCLC cells through regulating PI3K/AKT signaling pathway by targeting PTEN, indicating that miR-92a may be an attractive target and prognostic marker for NSCLC.

MiR-129 regulates cisplatin-resistance in human gastric cancer cells by targeting P-gp.

Development of multiple drug resistance (MDR) to chemotherapy is the major reason for the failure of gastric cancer (GC) treatment. P-glycoprotein (P-gp), which is encoded by MDR gene 1, as one of the mechanisms responsible for MDR. Mounting evidence has demonstrated that the drug-induced dysregulation of microRNAs (miRNAs) function may mediate MDR in cancer cells. However, the underling mechanisms of miRNA-mediated MDR in GC remain unclear. Here, we found that miR-129 was downregulated in cisplatin-resistant GC tissues/cells. Our results also showed that overexpression of miR-129 decreased cisplatin-resistance in cisplatin-resistant GC cells, and miR-129 knockdown reduced chemosensitivity to cisplatin in cisplatin-sensitive GC cells. Furthermore, miR-129 activated the intrinsic apoptotic pathway via upregulating caspase-9 and caspase-3. Most importantly, we further confirmed that P-gp is the functional target of miR-129 by regulating cisplatin-resistance in GC cells. These results suggested that miR-129 reversed cisplatin-resistance through inhibiting the P-gp expression in GC cells.

Upregulated long non-coding RNA BC032469 enhances carcinogenesis and metastasis of esophageal squamous cell carcinoma through regulating hTERT expression.

Currently, long non-coding RNAs (lncRNAs) have been shown to have critical regulatory roles in various cancers. However, its role in esophageal squamous cell carcinoma (ESCC) remains largely unknown. Here, we focused on lncRNA BC032469, one of the lncRNAs involved in the development of ESCC. The levels of a specific differentially expressed lncRNA (termed lncRNA-BC032469) were measured in 45 paired esophageal squamous cell carcinoma tissue samples by quantitative real-time RT-PCR and then subjected to correlation analysis with clinical parameters and prognosis. The functions of lncRNA-BC032469 were evaluated by silencing and overexpressing the lncRNA in vitro and in vivo. The expression level of BC032469 in esophageal squamous cell carcinoma tissues was higher than that in the corresponding non-cancerous tissues. High BC032469 levels were correlated with lymph node metastasis, TNM stage, and tumor size and lower overall survival. Knockdown of BC032469 in TE13 and Eca109 cells inhibited cell proliferation, migration, and invasion; induced cell cycle arrest in the G0/G1 phase; and promoted apoptosis. Western blot analysis revealed that BC032469 regulated the expression of human telomerase reverse transcriptase (hTERT), which is important for cell proliferation and metastasis. Moreover, the restored expression of hTERT protein in BC032469-knockdown cells attenuated the suppressive effects of BC032469 on ESCC cells. Collectively, these results indicated that lncRNA-BC032469 is an oncogenic lncRNA that promotes tumor progression and leads us to propose that lncRNAs may serve as key regulatory hubs in ESCC development.

Identification of differentially expressed genes between lung adenocarcinoma and lung squamous cell carcinoma by gene expression profiling.

The present study aimed to identify the differentially expressed genes (DEGs) between lung adenocarcinoma and normal lung tissues, and between lung squamous cell carcinoma and normal lung tissues, with the purpose of identifying potential biomarkers for the treatment of lung cancer. The gene expression profile (GSE6044) was downloaded from the Gene Expression Omnibus database, which included data from 10 lung adenocarcinoma samples, 10 lung squamous cell carcinoma samples, and five matched normal lung tissue samples. After data processing, DEGs were identified using the Student's t­test adjusted via the Benjamini­Hochberg method. Subsequently, Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis of the DEGs was performed using the Database for Annotation, Visualization and Integrated Discovery, and a global network was constructed. A total of 95 upregulated and 241 downregulated DEGs were detected in lung adenocarcinoma samples, and 204 upregulated and 285 downregulated DEGs were detected in lung squamous cell carcinoma samples, as compared with the normal lung tissue samples. The DEGs in the lung squamous cell carcinoma group were enriched in the following three pathways: Hsa04110, Cell cycle; hsa03030, DNA replication; and hsa03430, mismatch repair. However, the DEGs in the lung adenocarcinoma group were not significantly enriched in any specific pathway. Subsequently, a global network of lung cancer was constructed, which consisted of 341 genes and 1,569 edges, of which the top five genes were HSP90AA1, BCL2, CDK2, KIT and HDAC2. The expression trends of the above genes were different in lung adenocarcinoma and lung squamous cell carcinoma when compared with normal tissues. Therefore, these genes were suggested to be crucial genes for differentiating lung adenocarcinoma and lung squamous cell carcinoma.