Terryowen9551

Furthermore, miR-140-5p expression increased in the lung cancer cells compared with the control cells following transfection with miR-140-5p mimic. Overexpressing miR-140-5p significantly suppressed the proliferative, invasive and migratory abilities of H460 and PC-9 cells, and stimulated cell apoptosis by upregulating the expression of cleaved-caspase-3. Notably, these effects were reversed following transfection with miR-140-5p inhibitor. miR-140-5p was predicted as a negative regulator of ZNF800, and ZNF800 knockdown significantly suppressed the proliferative and metastatic abilities of lung adenocarcinoma (LUAD) cells, which was comparable to the effects of miR-140-5p mimic. Taken together, these results suggest that miR-140-5p may block the malignant phenotype of LUAD by negatively regulating ZNF800 expression. Thus, the miR-140-5p/ZNF800 axis may be used as an alternative therapeutic target for lung carcinoma in general, and LUAD in particular.Colorectal cancer (CRC) is the third most common malignant type of tumor worldwide. Selleck EN460 Neurensin-2 (NRSN2) is a small neuronal membrane protein associated with tumorigenesis. Therefore, the present study aimed to investigate the association between NRSN2 and CRC, and further examined the underlying mechanism of its effect on CRC metastasis. Human CRC SW620 cells were used to determine the biological functions of NRSN2 in CRC. Cell counting Kit-8 (CCK8), colony formation, wound-healing and transwell assays were performed to evaluate the role of NRSN2 on survival and metastasis of SW620 cells. The interaction between NRSN2 and SOX12 was determined via bioinformatics analysis and confirmed using immunoprecipitation. It was identified that NRSN2 was highly expressed in CRC cells and served a critical role in CRC cell survival compared with in healthy colon epithelial cells. Furthermore, NRSN2-knockdown inhibited the proliferation, invasion and migration of SW620 cells, while NRSN2 overexpression promoted these cellular processes. Additionally, it was demonstrated that NRSN2 could recruit SOX12 in SW620 cells. NRSN2-knockdown decreased SOX12 expression, while NRSN2 overexpression upregulated SOX12 expression. Overall, the present results suggested NRSN2 as a novel biomarker for CRC diagnosis and identified NRSN2 as a potential therapeutic target for CRC treatment.Hypoxia facilitates the progression of numerous cancers. Circular RNAs (circRNA) have been revealed to be involved in the process of tumors mediated by hypoxia. However, the role and molecular mechanism of circular RNA hsa_circ_0008450 (circ_0008450) in hepatocellular cancer (HCC) under hypoxic conditions has been rarely reported. Expression levels of circ_0008450, microRNA(miR)-431 and A-kinase anchor protein 1 (AKAP1) were examined using reverse transcription-quantitative PCR. Cell viability, apoptosis and glycolysis were assessed via Cell Counting Kit-8, flow cytometry and glycolysis assays, respectively. The association between circ_0008450 or AKAP1 and miR-431 was verified via dual-luciferase reporter assays. Protein levels of AKAP1 were detected by western blotting. Effect of hsa_circ_0008450 on tumor growth in vivo was confirmed by xenograft assays. Circ_0008450 was upregulated in HCC tissues and hypoxia-disposed HCC cells. Depletion of circ_0008450 suppressed tumor growth in vivo and reversed the repression of apoptosis and the acceleration of viability and glycolysis of HCC cells induced by hypoxia treatment in vitro. Notably, circ_0008450 regulated AKAP1 expression by sponging miR-431. Furthermore, miR-431 inhibition reversed the circ_0008450 silencing-mediated effects on viability, apoptosis and glycolysis in hypoxia-treated HCC cells. Additionally, AKAP1 enhancement abolished the effects of miR-431 upregulation on the viability, apoptosis and glycolysis in hypoxia-treated HCC cells. In conclusion, circ_0008450 repression mitigated the progression of HCC under hypoxia by downregulating AKAP1 via miR-431, providing a potential target for HCC treatment.Esophageal squamous cell carcinoma (ESCC) is one of the deadliest cancer types with a poor prognosis due to the lack of symptoms in the early stages and a delayed diagnosis. The present study aimed to identify the risk factors significantly associated with prognosis and to search for novel effective diagnostic modalities for patients with early-stage ESCC. mRNA and methylation data of patients with ESCC and the corresponding clinical information were downloaded from The Cancer Genome Atlas (TCGA) database, and the representation features were screened using deep learning autoencoder. The univariate Cox regression model was used to select the prognosis-related features from the representation features. K-means clustering was used to cluster the TCGA samples. Support vector machine classifier was constructed based on the top 75 features mostly associated with the risk subgroups obtained from K-means clustering. Two ArrayExpress datasets were used to verify the reliability of the obtained risk subgroups. The dif the joint representation learning-based model had good robustness, and had prognostic significance for patients with ESCC.Dysregulated microRNAs (miRNAs) serve vital roles in the progression and prognosis of breast cancer. miR-623 has been reported to influence the progression of numerous other cancers, such as lung adenocarcinoma and hepatocellular carcinoma, however, its role in breast cancer remains unclear. In the present study, the mRNA expression of miR-623 was studied in 121 pairs of breast cancer and adjacent normal tissues and cultured cell lines by reverse-transcription quantitative PCR. The association between miR-623 expression and clinical characteristics or the overall survival rate of patients was investigated by the χ2 test or Cox regression analysis, respectively. The role of miR-623 in cell proliferation, migration and invasion of breast cancer cells was evaluated by cell transfection to regulate miR-623 expression and the CCK8 and Transwell assays, respectively. miR-623 was downregulated in breast cancer tissues and cell lines compared with normal tissues and breast epithelial cell lines. The χ2 test demonstrated that the downregulation of miR-623 was associated with the tumor node metastasis (TNM) stage of patients with breast cancer.