Background: Cervical anastomotic leakage (CAL) is one of the most common complications that occur minimally invasive esophagectomy (MIE). It is associated with high postoperative mortality. Some risk factors still remained controversial and so accurate prediction of risk groups for CAL remained very difficult. This study aimed to identify the risk factors of CAL after McKeown MIE to predict the accuracy of the technique as early as possible. Material and Methods: A total of 129 patients with esophageal cancer who underwent McKeown MIE at the Department of Thoracic Surgery, the Fourth Hospital of Hebei Medical University, between January 2018 and June 2019 were retrospectively reviewed. Multivariate logistic regression analysis was used to identify the risk factors for CAL and receiver operating characteristic (ROC) curve analysis was used to predict the accuracy for each quantitative data variable and determine the cutoff value. Results: There were statistically significant differences between Group CAL and Group NCAL in FEV 1 (p = 0.031), neoadjuvant chemotherapy (p = 0.001), intraoperative minimum PaCO 2 (p = 0.002), and hospital stays (p <0.001). In multivariate logistic regression, FEV 1 (OR = 0.440, p = 0.047), neoadjuvant chemotherapy (OR = 4.425, p = 0.003), and intraoperative minimum PaCO 2 (OR = 1.14, p <0.001) were identified to be three risk factors of CAL. The ROC curve analysis showed that FEV 1 <2.18L (p = 0.029) and intraoperative minimum PaCO 2 >45.5 mmHg (p = 0.002) demonstrated good accuracy. Conclusion: FEV 1 , neoadjuvant chemotherapy, and intraoperative minimum PaCO 2 in arterial blood gas (ABG) were considered as risk factors of CAL after McKeown MIE for esophageal cancer. Preoperative FEV 1 <2.18L and intraoperative minimum PaCO 2 >45.5 mmHg in ABG showed good accuracy in predicting risk factors for CAL.
MicroRNAs (miRNAs) have been revealed to play a crucial role in oncogenesis of esophageal squamous cell carcinoma (ESCC). However, the biological role of miR-181a-5p in ESCC is currently less explored. The current study was designed to assess whether miR-181a-5p affects ESCC progression and further investigate relevant underlying mechanisms. Based on the data of GSE161533, GSE17351, GSE75241 and GSE67269 downloaded from GEO database, MAP2K1 (MEK1) was revealed to be one overlapping gene of the top 300 DGEs. Additionally, using the predicting software, miR-181a-5p was projected as the presumed target miRNA. Immunohistochemical staining and RT-qPCR research revealed that miR-181a-5p expression was decreased in human tumor tissues relative to surrounding peri-cancerous tissues. In an in vivo experiment, miR-181a-5p mimics could inhibit tumor growth and metastasis of ESCC. Gene expression profiles in combination with gene ontology (GO) and KEGG pathway analysis revealed that MAP2K1 (MEK1) gene and ERK-MMP pathway were implicated in ESCC progression. MiR-181a-5p mimics inhibited the activity of p-ERK1/2, MMP2 and MMP9 in vivo , as shown by Western blotting and immunohistochemistry labeling. There were no variations in the expression of p-P38 and p-JNK proteins. Additionally, miR-181a-5p mimics lowered p-ERK1/2, MMP2 and MMP9 levels in ECA109 cells, which were restored by MEK1-OE lentivirus. MEK1-OE Lentivirus significantly reversed the function induced by miR-181a-5p mimics in ECA109 cells. Moreover, further investigation indicated that the capability of migration, invasion and proliferation was repressed by miR-181a-5p mimics in ECA109 cells. In short, repressed ERK-MMP pathway mediated by miR-181a-5p can inhibit cell migration, invasion and proliferation by targeting MAP2K1 (MEK1) in ESCC.
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