Objective. To investigate miR-18a-5p and ataxia telangiectasia muted (ATM) expression in esophageal squamous cell carcinoma (ESCC) and their correlations with clinicopathological features. Methods. The subjects of this study were 62 ESCC patients (research group, RG) and 57 healthy controls (control group, CG) presented to our hospital between July 2019 and April 2020. Peripheral blood (PB) miR-18a-5p and ATM levels in these participants were quantified via qRT-PCR, and the correlations of the two genes with ESCC patients’ clinicopathological characteristics were investigated. In addition, a two-year follow-up was performed on ESCC patients to understand their survival, so as to further determine the prognostic utility of miR-18a-5p and ATM in ESCC. Factors influencing patient outcomes were identified by COX analysis. Results. PB miR-18a-5p expression was higher in RG compared with CG, while ATM was lower, suggesting an inverse connection between the two genes in ESCC ( P < 0.001 ). miR-18a-5p and ATM levels were determined to be strongly linked to TNM stage, differentiation degree, and lymph node metastasis in ESCC patients ( P < 0.001 and P = 0.007 ). The patients who succumbed to the disease exhibited higher miR-18a-5p and lower ATM than the survival ( P < 0.05 ). ROC analysis suggested favorable evaluation effects of miR-18a-5p and ATM on the occurrence and prognostic death of ESCC ( P < 0.001 ). Further, these two genes were identified by the COX analysis to be factors independently affecting the prognosis of ESCC. Conclusion. miR-18a-5p is highly expressed in ESCC, and ATM is underexpressed, both of which are closely linked to the pathological process of ESCC and have a good evaluation effect on the occurrence and prognosis of ESCC, which may become a breakthrough in future diagnosis and treatment of ESCC.

HFC125 is a potential substitutive to SF 6 in terms of its protective effectiveness, reduced GWP and cost. In the present study, corrosivity of HFC125 containing nitrogen atmosphere to the medium-carbon steel of C45E4 was examined by systematic experiments under the temperatures and HFC125 concentrations commonly used in Mg die-casting practice. For comparison, the corrosivity of SF 6 containing nitrogen atmosphere was examined in the identical conditions, followed by X-ray diffraction and X-ray fluorescence characterization of the corrosion products. The results show that the HFC125 containing nitrogen atmosphere was less corrosive to C45E4 than SF 6 containing one in long-playing corrosion under identical conditions. Oxidation was the major cause of the corrosion to C45E4 and HFC125 or SF 6 was of secondary contribution. HFC125 or its decomposition was deduced to corrode C45E4 to produce fluorides; SF 6 or its decomposition was deduced to react with C45E4 to produce sulfides.

Aberrant expression of microRNA‐497 (miR‐497) is associated with tumor progression, but the molecular mechanisms in tumorigenesis remain largely unknown. Here, we report that miR‐497 expression is downregulated in esophageal squamous cell carcinoma (ESCC) clinical samples. Consistently, upregulation of miR‐497 inhibits ESCC cell malignant properties and tumor growth in vivo. Importantly, we uncovered that miR‐497 upregulation suppressed ESCC cell growth and tumor growth by inhibiting Smurf2. Mechanistically, we showed that Smurf2 was a target of miR‐497, and mediated YY1 expression to elevate HIF2α expression, thereby enhancing the malignancy of ESCC cells. Together, our study uncovered the role of the miR‐497‐mediated Smurf2/YY1/HIF2α axis in tumor growth and metastasis, which might provide potential therapeutic targets for human ESCC.

Background It has been revealed that aging plays crucial roles in tumorigenesis, prognosis, and therapy response of tumors including esophageal carcinoma (ESCA). In this work, we aim to establish an aging-relevant risk signature to assess the survival outcome and immunogenicity status of ESCA patients. Methods A total of 351 ESCA patients with both gene expression data and clinical information from 3 independent datasets were curated. The Lasso-Cox regression model was applied to identify the aging genes that contributed most to the survival outcome. The risk signature was constructed by combining the specific gene expression level with the corresponding regression coefficients. Microenvironment-based immunologic factors, mutational burden, and significantly mutated genes were evaluated based on the identified risk groups. One cohort under the immune checkpoint inhibitor (ICI) treatment was used to investigate the immunotherapy predictive roles of the determined aging signature. Results Based on the 22 aging-relevant genes, a risk signature was constructed. ESCA patients with low-risk scores had improved survival outcomes in both discovery and validation datasets. Subsequent immunologic exploration demonstrated that the enhanced infiltration abundance of immune-response cells, decreased abundance of immune-suppressive cells, immune response-related signals, and the preferable ICI indicator enrichment were found in the low-risk group. Genomic mutation analysis showed the elevated mutational burden and increased mutation rates of significantly mutated genes of TP53, NAV3, and FAT1 were observed in patients with low-risk scores. In the ICI-treated cohort, we noticed that low-risk aging scores were significantly linked to favorable treatment outcomes and elevated response rates. Conclusions In summary, our identified aging risk signature showed the associations with survival, immune microenvironment, immunogenicity, and especially, the immunotherapy efficacy, which offers the clues for guiding prognosis evaluation and immune treatment strategies, and promotes precision therapy of ESCA patients.