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Background: Esophageal squamous cell carcinoma (ESCC) is a highly prevalent type of esophageal cancer (EC), usually found at an advanced stage with a high mortality rate, and it is now crucial to find new ways to diagnose and treat ESCC. This study analyzed the function of circular RNA_0003340 (circ_0003340)/microRNA‐940 (miR‐940)/protein kinase AMP‐activated alpha 1 catalytic subunit (PRKAA1) axis in ESCC. Methods: Circ_0003340, miR‐940 and PRKAA1 contents were measured with the application of real‐time quantitative polymerase chain reaction (RT‐qPCR) and western blot. Cell proliferation, cell cycle, apoptosis, migration, invasion and angiogenesis were assessed with a cell counting kit‐8 (CCK8), 5‐ethynyl‐2′‐deoxyuridine (EdU), flow cytometry, wound healing, transwell and tube formation assays. We used both the luciferase reporter system and RNA immunoprecipitation (RIP) to analyze the relationship between miR‐940 and circ_0003340 or PRKAA1. Finally, xenograft models were applied to analyze the effect of circ_0003340 on tumor growth in vivo. Results: Upregulated circ_0003340 and PRKAA1, and downregulated miR‐940 levels were detected in ESCC. Meanwhile, ESCC progression was apparently restrained by circ_0003340 knockdown in vitro. Circ_0003340 acted as a ceRNA for miR‐940 in regulating ESCC progression and miR‐940 was proved to target PRKAA1 to arrest ESCC progression in vitro. Finally, in vivo experiments established that silencing of circ_0003340 slowed tumor growth in vivo. Conclusion: Circ_0003340 downregulation mitigated esophageal squamous cell carcinoma progression by targeting miR‐940/PRKAA1 axis. [ABSTRACT FROM AUTHOR]

Background: Esophageal squamous cell carcinoma (ESCC) is one of the most lethal malignancies. Latest studies report that long noncoding RNAs (LncRNAs) play an essential role in diversified pathological processes of ESCC, although the mechanism by which they do so remains unknown. This study aimed to explore the parts of lncRNA taurine upregulated gene 1 (TUG1) in ESCC tissues and cells, its biofunctional effect and its underlying regulatory mechanism in ESCC. Methods: The levels of TUG1 and miR‐148a‐3p were detected by quantitative real‐time polymerase chain reaction (qRT‐PCR) in ESCC cells and tissues. The biofunctional effects were examined by MTT, flow cytometry, and transwell assay. The protein expression levels of epithelial‐mesenchymal transition (EMT)‐related proteins and MCL‐1 were determined by western blot analysis. The binding sites between miR‐148a‐3p and TUG1 or MCL‐1 were predicted by online software starBase and confirmed by dual luciferase reporter assay. Results: The mRNA expression of TUG1 was significantly upregulated in ESCC tissues or cells, and was negatively correlated to miR‐148a‐3p expression in tissues. Knockdown of TUG1 inhibited the proliferation, migration, and invasion, promoted apoptosis, and relieved the EMT progression in EC9706 and OE19 cells. Besides, knockdown of miR‐148a‐3p inverted positive effects from TUG1 deletion on ESCC cells. Besides, MCL‐1 reversed the inhibitive effects from TUG1 deletion on expression of EMT‐associated proteins (Wnt1, C‐myc, CyclinD1, and β‐catenin) above subsequently. Conclusion: TUG1 regulated the biofunction and EMT progression of ESCC by mediating miR‐148a‐3p/MCL‐1/Wnt/β‐catenin axis in vitro. [ABSTRACT FROM AUTHOR]

Background Micro ribonucleic acid ( miR-101) can regulate the expression of cyclooxygenase-2 ( COX-2) and participate in the pathogenesis of malignant tumors. This study investigates the effects of miRNA-101 and COX-2 in lung cancer and the impact of miR-101 on the proliferation and invasion of human lung cancer A549 cell line. Methods The expression of miR-101 in 20 separate lung cancer tissues was detected by real time polymerase chain reaction; COX-2 expression was also detected. A549 cells were transfected with miR-101 or negative control oligonucleotide duplex mimic ( miR- NC). In vivo tumorigenesis abilities were detected in localized human lung cancer xeno-transplant models in BALB/c nude mice. Results MiR-101 expression was significantly lower and the level of COX-2 significantly higher in lung cancer tissues than in adjacent parenchyma (2.918 ± 1.006 vs. 5.953 ± 1.976, P = 0.001; 0.887 ± 0.260 vs. 0.355 ± 0.156, P = 0.001, respectively). Correlation analysis revealed that miR-101 negatively correlated with COX-2 in lung cancer tissues (R = −0.596, P = 0.002). Compared with A549- miR- NC cells, the expression of COX-2 was significantly decreased in A549 cells transfected with miR-101 ( P < 0.001). The proliferation of A549 cells was markedly inhibited after transfection of miR-101. The in vivo tumor growth of A549 cells transfected with miR-101 was significantly slower than wide type A549 cells. Conclusion MiR-101 expression is decreased in lung cancer, inducing an increase in COX-2 level. Enforced expression of miR-101 can remarkably reduce the cell proliferation and invasion ability of lung cancer cells. [ABSTRACT FROM AUTHOR]

Background To determine the relationship between FOXN1 (a transcription factor) and B cell-attracting chemokine 1 ( BCA1, a chemotactic factor), and their influence on thymoma cell proliferation. Methods We initially used immunohistochemical methods to compare the expression levels of FOXN1 and BCA1 in thymoma and non-thymomatous tissue samples. Reverse transcription polymerase chain reaction ( RT-PCR) and Western blotting were used to compare the expression of FOXN1 and BCA1 in thymoma cells ( Thy0517) and normal thymic epithelial cells ( CRL7660). We used ribonucleic acid interference ( RNAi) to downregulate FOXN1 and BCA1 expression in Thy0517 cells to determine the relationship of the two factors with cell regulation. We also performed methyl thiazolyl tetrazolium ( MTT) [3-(4,5)-dimethylthiahiazo(-z-y1)-3,5-di-phenytetrazoliumromide] assays to detect the changes in Thy0517 cells after RNAi of FOXN1 and BCA1. Results FOXN1 and BCA1 expression levels were higher in thymoma tissues and Thy0517 cells compared to non-thymomatous tissue and CRL7660 cells ( P < 0.05). RT-PCR and Western blot following RNAi showed that FOXN1 controlled BCA1 expression. MTT assay showed that FOXN1 and BCA1 downregulation rapidly inhibited Thy0517 cell proliferation. Conclusions FOXN1 and BCA1 expression was higher in thymoma tissue samples and cell lines than in non-thymomatous tissue and normal thymic epithelial cells. FOXN1 acts upstream of BCA1 and both FOXN1 and BCA1 promote thymoma cell proliferation. [ABSTRACT FROM AUTHOR]

Background A high expression of squalene epoxidase ( SQLE) is related to tumor occurrence, development, and prognosis in a variety of cancers. In this study, the expression and significance of SQLE was analyzed in patients with squamous lung cancer and pericarcinoma tissues. Methods The SQLE mRNA and protein expression were separately examined by semi-quantitative reverse transcription polymerase chain reaction, fluorescence quantitative polymerase chain reaction and Western blot in 65 cases of squamous cell lung carcinoma tissues and adjacent non-cancerous lung tissues. Results The expression of SQLE mRNA and protein in lung squamous cancerous tissues was significantly higher than in pericarcinoma tissues (63.07% vs. 44.61%, P = 0.0348; 67.69% vs. 38.46%, P = 0.0008). The positive expression rate of SQLE mRNA was not associated with gender, age, smoking, or tumor size ( P > 0.05). The expression of SQLE mRNA was closely correlated with poor differentiation, clinical stages, and lymphatic metastasis ( P < 0.05). The expression of SQLE mRNA was negatively associated with overall survival rate ( P < 0.05). Conclusion A high expression of SQLE was found in squamous lung cancer tissues. The high expression of the SQLE gene may be closely related to the occurrence and development of squamous cell lung carcinoma. SQLE expression predicts a poor prognosis and may serve as a novel lung carcinoma molecule marker. [ABSTRACT FROM AUTHOR]