Search

Lung adenocarcinoma (LUAD) accounts for ~40% of lung cancer cases, and the 5‐year relative survival rate is no more than 1%. Dysregulation of components of striatin‐interacting phosphatase and kinase (STRIPAK) complexes is associated with various diseases, including cancer. Striatin‐interacting protein 2 (STRIP2), also called Fam40b, has been reported to regulate tumor cell growth and migration. Here, we investigated the role of STRIP2 in LUAD growth, migration and the underlying mechanisms. Analysis of data from The Cancer Genome Atlas database revealed that STRIP2 is highly expressed and predicted poor outcomes in patients with LUAD. Moreover, quantitative RT‐PCR (qRT‐PCR) analysis revealed that the mRNA expression of STRIP2 is greater in all tested LUAD cells than in a normal lung cell line. To investigate the function of STRIP2, we overexpressed STRIP2 in SPC‐A1 cells and depleted STRIP2 in Calu‐3 cells. Cell proliferation was evaluated by Cell Counting Kit‐8 and colony‐forming assays, and Transwell assay was employed to test cell invasion and migration. Our results indicate that STRIP2 depletion suppressed cell proliferation, invasion and migration in Calu‐3 cells, and overexpression of STRIP2 had the opposite effects in SPC‐A1 cells. Moreover, we discovered that STRIP2 depletion reduced the protein levels of p‐Akt and phosphorylated‐mammalian target of rapamycin (p‐mTOR) in Calu‐3 cells, whereas STRIP2 overexpression increased levels of these proteins in SPC‐A1 cells. Furthermore, we found that silencing of STRIP2 clearly enhanced protein levels of E‐cadherin and reduced levels of N‐cadherin, Vimentin and matrix metalloproteinase‐9 in Calu‐3 cells, whereas overexpression of STRIP2 had the opposite effect in SPC‐A1 cells. Our data indicate that STRIP2 promotes the proliferation and motility of LUAD cells, and this may be mediated through the regulation of the Akt/mTOR pathway and epithelial–mesenchymal transition. These results may facilitate the development of therapeutic strategies to treat LUAD., Striatin‐interacting protein 2 has been reported to regulate tumor cell growth and migration. Our data indicate that Striatin‐interacting protein 2 promotes the proliferation, invasion and migration of lung adenocarcinoma cells, and this may be mediated through regulation of the Akt/mTOR pathway and epithelial–mesenchymal transition.

Background:The aim of this study was to analyze the profile of chest injuries, oxygen therapy for respiratory failure, and the outcomes of victims after the Jiangsu tornado, which occurred on June 23, 2016 in Yancheng City, Jiangsu Province, China.Methods:The clinical records of 144 patients referred to Yancheng City No.1 People’s Hospital from June 23 through June 25 were retrospectively investigated. Of those patients, 68 (47.2%) sustained major chest injuries. The demographic details, trauma history, details of injuries and Abbreviated Injury Scores (AIS), therapy for respiratory failure, surgical procedures, length of intensive care unit (ICU) and hospital stay, and mortality were analyzed.Results:Of the 68 patients, 41 (60.3%) were female and 27 (39.7%) were male. The average age of the injured patients was 57.1 years. Forty-six patients (67.6%) suffered from polytrauma. The mean thoracic AIS of the victims was calculated as 2.85 (SD = 0.76). Rib fracture was the most common chest injury, noted in 56 patients (82.4%). Pulmonary contusion was the next most frequent injury, occurring in 12 patients (17.7%). Ten patients with severe chest trauma were admitted to ICU. The median ICU stay was 11.7 (SD = 8.5) days. Five patients required intubation and ventilation, one patient was treated with noninvasive positive pressure ventilation (NPPV), and four patients were treated with high-flow nasal cannula (HFNC). Three patients died during hospitalization. The hospital mortality was 4.41%.Conclusions:Chest trauma was a common type of injury after tornado. The most frequent thoracic injuries were rib fractures and pulmonary contusion. Severe chest trauma is usually associated with a high incidence of respiratory support requirements and a long length of stay in the ICU. Early initiation of appropriate oxygen therapy was vital to restoring normal respiratory function and saving lives. Going forward, HFNC might be an effective and well-tolerated therapeutic addition to the management of acute respiratory failure in chest trauma.

Objective. Esophageal cancer (ESCC) is reported to be the eighth most common malignant tumors worldwide with high mortality. However, the functions of majority circRNAs in ESCC requires to be further explored. Methods. This study identified differently expressed circRNAs in 3 paired ESCC using RNA-sequencing method. The interactions among circRNAs, miRNAs, and mRNAs were predicted using bioinformatics analysis. Results. In this study, using RNA-sequencing method and integrated bioinformatics analysis, 418 overexpressed circRNAs and 637 reduced circRNAs in ESCC sample were identified. Based on the mechanism that circRNAs could play as ceRNAs to modulate targets expression, circRNA-miRNA and circRNA-miRNA-mRNA networks were constructed in this study. Based on the network analysis, 7 circRNAs, including circ_0002255, circ_0000530, circ_0001904, circ_0001005, circ_0000513, circ_0000075, and circ_0001121, were identified as key circRNAs in ESCC. We found that circ_0002255 was related to the regulation of substrate adhesion-dependent cell spreading. circ_0001121 was involved in regulating nucleocytoplasmic transport. circ_0000513 played a key role in regulating Adherens junction, B cell receptor signaling pathway. Meanwhile, we observed circ_0000075 was involved in regulating zinc II ion transport, transition metal ion homeostasis, and angiogenesis. Conclusion. We thought this study could provide novel biomarkers for the prognosis of ESCC.