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Impulsive pneumomediastinum being an unconventional complications involving COVID-19 pneumonia.
Objective The aim of this study was to investigate the expression of long non-coding ribonucleic acid (lncRNA) AK058003 in esophageal carcinoma (EC) tissues, and to analyze its intervention effect. Patients and methods The expression of lncRNA AK058003 in EC tissues and para-carcinoma tissues from 130 EC patients was detected via quantitative Polymerase Chain Reaction (qPCR). EC cell lines were selected for exogenous interference in lncRNA AK058003. Subsequently, the expression of lncRNA AK058003 in normal esophageal epithelial cell line (Het-1A) and EC cell lines (EC109, EC9706, KYSE-150, KYSE-30, and TE-1) was detected by qPCR. EC9706 cell lines with the highest expression of lncRNA AK058003 were selected and transfected with lncRNA AK058003 siRNA and lncRNA AK058003 control, respectively. After transfection, the expression of lncRNA AK058003 was determined using PCR. The changes in cell growth and proliferation were analyzed via cell growth curve and cell cycle assay. Meanwhile, the changes in cell migrati in lncRNA AK058003 siRNA group. Wound healing assay indicated that the intercellular distance became large, and cell migration ability was evidently enhanced in lncRNA AK058003 siRNA group with time (p less then 0.05). Besides, the protein expressions of MMP1 and MMP2 were remarkably lower in lncRNA AK058003 siRNA group than those in lncRNA AK058003 control group. This indicated remarkably declined invasion and metastasis ability. In addition, the postoperative prognosis was significantly worse in patients with higher expression of lncRNA AK058003 (p less then 0.05). All these findings suggested that lncRNA AK058003 could serve as a biomarker for EC prognosis. Conclusions LncRNA AK058003 is highly expressed in EC patients, which promotes proliferation, migration, invasion, and metastasis of EC cells. In addition, the postoperative prognosis of EC patients with high expression of lncRNA AK058003 is relatively poor.Objective Esophageal squamous cell carcinoma (ESCC) is a common malignant epithelial tumor in the elderly, and the cause is very complicated. Therefore, the study of the pathogenesis of ESCC is conducive to the effective treatment of ESCC. Many studies indicated that lncRNAs were important regulatory factors in tumor formation and disease development. However, the regulatory network of lncRNA in ESCC has not been fully explored. Materials and methods The expression of miR-574-3p, ZEB2-AS1, and HMGA2 was measured using qRT-PCR. The protein expression of PCNA, Cleaved-caspase3, MMP9, and HMGA2 was detected through Western blot. Cell proliferation or apoptosis of transfected cells was calculated via CKK-8 assay or flow cytometry. Transwell assay was applied to detect cell migration and invasion of ESCC cells. Luciferase reporter assay and RNA pull-down were used to determine the relationship among miR-574-3p, ZEB2-AS1, and HMGA2 in ESCC. Moreover, the regulatory network of ZEB2-AS1 has been verified in vivo in this study. Results We found that ZEB2-AS1 was upregulated in ESCC tissues and cells. The knockdown of ZEB2-AS1 could inhibit cell proliferation, invasion, and migration, as well as promoted cell apoptosis in ESCC. Interestingly, miR-574-3p deficiency or HMGA2 promotion could reverse the effects of si-ZEB2-AS1 on ESCC cell progression. Luciferase reporter assay indicated that miR-574-3p was a target miRNA of ZEB2-AS1 and HMGA2 was a target gene of miR-574-3p in ESCC. Conclusions In this paper, we first verified the novel regulatory mechanism of lncRNA ZEB2-AS1 in ESCC cellular process. LncRNA ZEB2-AS1 promoted the proliferation, migration, and invasion of ESCC by modulating miR-574-3p/HMGA2 axis, indicating that ZEB2-AS1 played essential roles in cell progression in ESCC and providing a new therapeutic target of ESCC.Objective Long noncoding RNAs (lncRNAs) display a functional effect on the pathogenesis of several diseases, including various tumors. Herein, we aimed to reveal the role of lncRNA somatostatin receptor 5 antisense RNA 1 (SSTR5-AS1) in gastric cancer (GC). Patients and methods qRT-PCR was utilized for testing the SSTR5-AS1 expression in 158 paired primary GC tissues and corresponding normal gastric specimens. Receiver operating characteristic (ROC) curves were established to determine the diagnostic values of overexpression of SSTR5-AS1 in GC. A chi-square test was performed to analyze the correlation between SSTR5-AS1 expressions and several clinicopathological features in GC patients. Kaplan-Meier survival curve was constructed to estimate the overall survival (OS) and disease-free survival (DFS). Multivariate analyses were conducted to examine the prognostic value of SSTR5-AS1. Results We observed that SSTR5-AS1 expression was highly expressed in GC specimens compared with adjacent non-tumor specimens (p less then 0.01). High SSTR5-AS1 expression was correlated with an advanced pathologic stage. Gilteritinib The ROC curves showed that areas under the ROC curve (AUC) for SSTR5-AS1 is 0.8419. Moreover, high expression of SSTR5-AS1 was observed to be associated with distant metastasis (p = 0.021) and TNM stage (p = 0.042). Besides, survival analysis showed that GC patients with high SSTR5-AS1 expression suffered poorer OS (p = 0.020) and DFS (p = 0.0007). Multivariate assays demonstrated that increased expressions of SSTR5-AS1 could be an independent prognostic marker of OS and DFS of GC patients. Conclusions Our findings indicate that SSTR5-AS1 served as a promising novel prognostic biomarker for GC.Objective Abundant evidence has demonstrated that long non-coding RNAs (lncRNAs) play key roles in the development of human neoplasms. A novel cancer-related lncRNA, leukemia inhibitory factor receptor antisense RNA 1 (LIFR-AS1), has been reported to be under-expressed in breast cancer and associated with poor prognosis, but its significance in gastric cancer (GC) remains to be determined. Therefore, we assessed the prognostic and diagnostic value of LIFR-AS1 in GC. Patients and methods Quantitative RT-PCR assay was used to detect the expression levels of LIFR-AS1 in GC tissues and adjacent normal tissues. The correlation between LIFR-AS1 expression and clinicopathological features was analyzed by Pearson's χ2-test. The disease-free survival and overall survival rates of GC patients were calculated by the Kaplan-Meier method. Cox regression analysis was used to assess factors related to survival. Results In this study, levels of LIFR-AS1 were significantly higher in GC tumor samples relative to adjacent normal tissue samples.
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