Zobrazení zdroje stránky Davisfernandez2599

The present study aimed to identify genes associated with gastric cancer survival and improve risk stratification for patients with gastric cancer. Transcriptomic and clinicopathological data from 443 gastric cancer samples were retrieved from The Cancer Genome Atlas database. The DESeq R package was applied to screen for differentially expressed genes between Tumor-Node-Metastasis (TNM) stage (I vs. IV) and histological grade (G3 vs. G1 and G2). A total of seven genes were common to both comparisons; spondin 1 (SPON1); thrombospondin 4 (THBS4); Sushi, Von Willebrand factor type A, EGF and pentraxin domain containing 1 (SVEP1); prickle planar cell polarity protein 1 (PRICKLE1); ATP binding cassette subfamily A member 8 (ABCA8); Slit guidance ligand 2 (SLIT2); and EGF containing fibulin extracellular matrix protein 1 (EFEMP1), were selected as candidate survival-associated genes for further analysis. The prognostic value of these genes was assessed according to a literature review and Kaplan-Meier survival analysis. In addition, a multivariate Cox regression analysis revealed PRICKLE1 expression to be an independent prognostic factor for patients with gastric cancer. Furthermore, a predictive nomogram was generated using PRICKLE1 expression, patient age and TNM stage to assess overall survival (OS) rate at 1, 3 and 5 years, with an internal concordance index of 0.65. External validation was conducted in an independent cohort of 59 patients with gastric cancer, and high consistency between the predicted and observed results for OS was exhibited. Overall, the current findings suggest that PRICKLE1 expression may serve as an independent prognostic factor that can be integrated with age and TNM stage in a nomogram able to predict OS rate in patients with gastric cancer.Understanding the different genetic landscape between lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC) is important for understanding the underlying molecular mechanism, which may facilitate the development of effective and precise treatments. Although previous studies have identified a number of differentially expressed genes (DEGs) responsible for lung cancer, it is unknown which of these genes are causal. The present study integrated DNA methylation, RNA sequencing, clinical characteristics and survival outcomes of patients with LUAD and LUSC from The Cancer Genome Atlas. DEGs were first identified using edgeR by comparing tumor and normal tissue, and differentially methylated probes (DMPs) were assessed using ChAMP. Candidate genes for further time-to-event instrumental variable analysis were selected as the intersecting genes between DEGs and the genes including DMP CpG sites within the transcription start site (TSS1500), with DMPs in TSS1500 region being the instrumental variables. Extensive sensitivity analyses were conducted to assess the robustness of the results. The present study identified 906 DEGs for LUAD, among which 538 also had DMPs in the TSS1500 region. In addition, 1,543 DEGs were identified for LUSC, among which 1,053 also had DMPs in the TSS1500 region. Time-to-event instrumental variable analysis detected eight potential causal genes for LUAD survival, including aryl hydrocarbon receptor nuclear translocator like 2, semaphorin 3G, serum deprivation-response protein, chloride intracellular channel protein 5, LIM zinc finger domain containing 2, epithelial membrane protein 2, carbonic anhydrase 7 and LOC116437. The results also identified that phosphatidylinositol-3,4,5-trisphosphate-dependent Rac exchange factor 2 may be a potential causal gene for LUSC. Therefore, the results of the present study suggested that there was molecular heterogeneity between these two lung cancer subtypes. Such analysis framework can be extended to other cancer genomics research.Methylation is a fundamental regulator of gene transcription. Long non-coding RNA maternally expressed 3 (MEG3) inhibits cell proliferation in various types of cancer. However, the molecular mechanisms of MEG3 methylation in the regulation of multiple myeloma (MM) are unknown. In the present study, MEG3 upregulation was negatively associated with the International Staging System (ISS) status of the bone marrow samples of 39 patients with MM. MEG3 overexpression in an MM cell line resulted in elevated p53 expression. Furthermore, the results of methylation-specific PCR revealed that the abnormal methylation status of the MEG3 promoter region was present in eight of the 39 bone marrow samples collected. Treatment of the MM cell line with the DNA methylation inhibitor 5-Aza-2'-deoxycytidine (5-Aza-CdR) resulted in tumor cell proliferation inhibition, apoptosis induction and G0/G1 cell cycle arrest. [https://www.selleckchem.com/products/ldn193189.html see more] Furthermore, 5-Aza-CdR decreased aberrant hypermethylation of the MEG3 promoter and increased the expression of MEG3. However, 5-Aza-CdR exerted no effect on p53 expression. To the best of our knowledge, the present study is the first to report that the demethylation reagent 5-Aza-CdR may serve as a therapeutic agent in MM by upregulating MEG3 expression. However, the mechanism of action was independent of p53 expression.Undaria pinnatifida (U. pinnatifida) polysaccharides (UPPS) are considered to be the major bioactive components of U. pinnatifida. The aim of the present study was to investigate the separation, sulfated modification, characterization and monosaccharide composition of UPPS. The optimal processing conditions were as follows Distilled water-to-solid ratio, 50 ml/g; extraction time, 300 min; and extraction temperature, 90˚C. The major polysaccharide fraction of U. pinnatifida (UPPS-B1) was purified via DEAE-52 and Sephadex G-200 column chromatography. The chlorosulfonic acid-pyridine method was applied for sulfation modification. UPPS-B1 and sulfated (S)-UPPS-B1 were characterized via chemical analysis, ultraviolet-visible and Fourier-transformed infrared spectroscopy, gas chromatography and high-performance liquid chromatography. The total sugar content of UPPS-B1 and S-UPPS-B1 was 79.78 and 77.28%, respectively. The sulfate radical content of UPPS-B1 and S-UPPS-B1 was 8.53 and 29.12%, whilst the content of uronic acid was 9.