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Sequencing, Phrase, along with Functional Studies of four Body's genes In connection with Essential fatty acid Biosynthesis In the Diapause Method within the Woman Ladybird, Coccinella septempunctata M.
The detection of certain oncogenic driver mutations, including those of epidermal growth factor receptor (EGFR), is essential for determining treatment strategies for advanced non-small cell lung cancer (NSCLC). The current study assessed the feasibility of testing exhaled breath condensate (EBC) for EGFR mutations by droplet digital PCR (ddPCR). Samples were collected from 12 patients with NSCLC harboring EGFR mutations that were admitted to Okayama University Hospital between June 1, 2014 and December 31, 2017. A total of 21 EBC samples were collected using the RTube™ method and EGFR mutations (L858R, exon 19 deletions or T790M) were assessed through ddPCR analysis (EBC-ddPCR). A total of 3 healthy volunteer samples were also tested to determine a threshold value for each mutation. Various patient characteristics were determined, including sex (3 males and 9 females), age (range 54-81 years; median, 66 years), smoking history (10 had never smoked; 2 were former smokers), histology (12 patients exhibited adenocarcinoma), clinical stage (9 patients were stage IV; 3 exhibited post-operative recurrence) and EGFR mutation type (4 had L858R; 8 had exon 19 deletions; 8 had T790M). EBC-ddPCR demonstrated positive droplets in 8 of the 12 patients. The sensitivity and specificity of each mutation was as follows 27.3 and 80.0% for EGFR L858R, 30.0 and 90.9% for EGFR Ex19del, and 22.2 and 100% for EGFR T790M. EBC-ddPCR analysis of EGFR mutations exhibited modest sensitivity and acceptable specificity. EBC-ddPCR is a minimally invasive and replicable procedure and may be a complementary method for EGFR testing in patients where blood or tissue sampling proves difficult.This study investigated the relationship of the expression of transient receptor potential channel 1 (TRPC1), small breast epithelial mucin (SBEM) in breast cancer tissues with clinical pathological features and prognosis of patients. Altogether 50 patients with breast cancer who were treated in Weifang People's hospital from April 2017 to November 2018 were selected, and the mRNA and protein differences of TRPC1 and SBEM in breast cancer patients and normal breast cancer tissues were detected by qRT-PCR and Western blot. Spearman test was used for correlation analysis. Logistic univariate and multivariate analysis were performed on the risk factors related to breast cancer metastasis in breast cancer patients. The expression of TRPC1 and SBEM in breast cancer tissues was significantly higher than that in normal breast tissues (P less then 0.001). The mRNA expression of TRPC1, SBEM and protein was not related to age, tumor size and tissue grade of breast cancer patients, but related to TNM stage, clinical stage and lymph node metastasis (P less then 0.001). The relative expression of TRPC1 was positively correlated with clinical stage of breast cancer (r=0.992, P less then 0.001). The relative expression of SBEM was positively correlated with the clinical stage of breast cancer (r=0.853, P less then 0.001). The relative expression of TRPC1 was positively correlated with TNM staging of breast cancer (r=0.860, P less then 0.001). The relative expression of SBEM was positively correlated with TNM staging of breast cancer (r=0.880, P less then 0.001). Multivariate conditional Logistic regression analysis showed that TNM staging, TRPC1, SBEM were independent risk factors for malignant breast cancer metastasis. On the contrary, expression of TRPC1 and SBEM in breast cancer tissues was up-regulated. TRPC1 and SBEM may be involved in the process of breast cancer occurrence, development and metastasis, and can be used as potential tissue biomarkers in diagnosis of breast cancer metastasis and disease assessment.Osteosarcoma is a common primary bone cancer that there are currently no effective treatment strategies for. Forkhead box M1 (FoxM1) is key in the development of osteosarcoma, and microRNA (miR)-216b serves an antitumor role by targeting FoxM1. Moreover, thiostrepton (TST), a natural thiazole antibiotic, induces antitumor effects and specifically targets FoxM1. Therefore, the present study investigated whether thiostrepton and miR-216b synergistically inhibited osteosarcoma cells by targeting FoxM1. The MTT assay, reverse transcription-quantitative PCR, a dual-luciferase reporter assay and flow cytometry were performed. Compared with the human osteoblast cell line hFOB1.19, miR-216b expression was significantly downregulated in the osteosarcoma cell lines U2OS, MG63 and Saos-2. By contrast, FoxM1 expression was significantly upregulated in osteosarcoma cell lines compared with the hFOB1.19 cell line. The results indicated that miR-216b targeted the 3'-untranslated region of FoxM1. Moreover, the results suggested that miR-216b cooperated with TST to decrease cell cytotoxicity and increase cell apoptosis. In addition, miR-216b cooperated with TST to increase Bax expression and decrease Bcl-2 expression. In conclusion, the combination of TST and miR-216b synergistically promoted osteosarcoma cell cytotoxicity and apoptosis by targeting FoxM1. Therefore, the present study suggested that the combination of TST and miR-216b may serve as a promising therapeutic strategy for osteosarcoma.Despite advances in the diagnosis and treatment in recent years, lung cancer is still one of the primary causes of cancer-associated morbidity and mortality in globally. Abnormally expressed microRNAs (miRNAs/miRs) in tumor tissues serve vital roles in the pathological mechanism of tumors and have become prospective biomarkers for cancer diagnosis. The present study aimed to investigate the effects of the miR-140-5p/zinc finger protein 800 (ZNF800) axis in lung carcinoma, and determine its potential underlying molecular mechanisms. The degree of cell proliferation was assessed via the MTT assay, while the migratory and invasive abilities of lung cancer cells were determined via the Transwell and Matrigel assays. The expression levels of miR-140-5p and ZNF800 were detected via reverse transcription-quantitative PCR and western blot analyses. The results demonstrated that miR-140-5p expression was notably higher in normal human bronchial epithelial cells compared with the respective lung cancer cell lines, H292, PC-9, CL1-5 and H460. 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. 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. AG-1024 cell line 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 differentially expressed genes and methylation genes (DEGs and DMGs) between the risk subgroups were analyzed, and pathway enrichment analysis was performed.
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