5 months for patients with mutation, and 19.5 months for patients without mutation (P=0.005). Positive expression of as shown by IHC was detected in majority of SRCC samples, which was higher than our intestinal cohort (28% 12.6%, P=0.033). We further explored the correlation between status and drug sensitivity in 4 SRCC cell lines. SNU601 and SNU668, which harbored mutation, were hypersensitive to MEK and mTOR inhibitors than wide type cell lines KATO-III and NUGC-4. Our findings demonstrate that gene plays an important role in SRCC and reveals therapeutic potential of targeting tumors by inhibiting MEK and mTOR pathways.Our findings demonstrate that KRAS gene plays an important role in SRCC and reveals therapeutic potential of targeting tumors by inhibiting MEK and mTOR pathways. The effect of microRNAs (miRNA) on cancer regulations has received a considerable amount of attention recently. MiR-133a-5p has been identified as an anti-tumor miRNA in several types of cancers. However, the effect of miR-133a-5p on gastric cancer (GC) have not been uncovered. In this study, we sought to evaluate the regulation of TCF4 expression by miR-133-5p and the role of the miR-25-3p/TCF4 axis in the progression of GC, with the aim of identifying a potential therapeutic target for GC. TCGA (The Cancer Genome Atlas), GTEx (The Genotype-Tissue Expression) and GEO (Gene Expression Omnibus) database were used to analyze the expression and prognosis. We performed MTT and EdU assays to elucidate the effect on cell replication. this website Apoptotic cells were stained with annexin V-fluorescein isothiocyanate and propidium iodide to stain, and then analyzed by flow cytometry. The effect on cell metastasis was investigated in wound healing and transwell assays. A dual-luciferase reporter assay was used to check for the direct targeting of TCF4 by miR-133a-5p. Bioinformatic analysis of the relationship of TCF4 with tumor microenvironment and the signaling cascade of TCF4 was finally performed. We found that the level of miR-133a-5p was decreased in both tumor tissues and GC cell lines. MiR-133a-5p inhibited cell growth and metastasis, but promoted cell apoptosis. MiR-133a-5p directly targeted TCF4 and downregulated its expression. TCF4 was highly expressed in tumor and higher level of TCF4 indicated poorer prognosis. Moreover, TCF4 overexpression reversed the aforementioned anti-tumor activity of miR-133a-5p. The expression level of TCF4 was significantly correlated with tumor-infiltrating immune cells. Our findings altogether reveal that miR-133a-5p can serve as a tumor suppressor in gastric cancer via the miR-133a-5p/TCF4 pathway.Our findings altogether reveal that miR-133a-5p can serve as a tumor suppressor in gastric cancer via the miR-133a-5p/TCF4 pathway. This study aimed to identify potential biomarkers associated with locoregional recurrence in patients with esophageal squamous cell carcinoma (ESCC) after radical resection. We performed a quantitative proteomics analysis using isobaric tags for relative and absolute quantification (iTRAQ) with reversed-phase liquid chromatography-mass spectrometry (RPLC-MS) to identify differential expression proteins (DEPs) between a locoregional recurrence group and good prognosis group of ESCC after radical esophagectomy. The bioinformatics analysis was performed with ingenuity pathway analysis software (IPA) and Gene Ontology (GO) database using the software of MAS 3.0. Kaplan-Meier (KM) Plotter Online Tool (http//www.kmplot.com) was used to evaluate the relationship between the differential expression of proteins and survival in patients with ESCC. More than 400 proteins were quantitated of which 27 proteins had upregulated expression and 55 proteins had downregulated expression in the locoregional recurrence grouwith large populations of ESCC to validate these potential biomarkers. This article aims to analyze the correlation between microvessel density (MVD) and multi-spiral CT(MSCT) perfusion parameters of esophageal cancer lesions, and the diagnostic value of combining C-terminal binding protein 2 (CtBP2) and P16 inhibitor of cyclin-dependent kinase 4a (P16 ). A total of 42 cases of normal esophageal mucosa tissues >5 cm from the cancer tissue were selected as the control group. The expression levels of CtBP2 and P16 and the values of MSCT perfusion parameters and MVD were compared in the control group and esophageal cancer group. SP immunohistochemical staining was used to detect protein expression levels of CtBP2 and P16 . The Pearson method was used to analyze the differences and pertinence of MSCT perfusion parameters and MVD in the control group and esophageal cancer group. The receiver operating characteristic (ROC) curve was used to calculate the diagnostic value of CtBP2 and P16 combined with MVD and MSCT perfusion parameters in esophageal cancer. The positive combined detection curve was larger, at 0.869. MSCT perfusion imaging of esophageal cancer lesions can indirectly reflect the angiogenesis of esophageal cancer, and the combination of CtBP2 and P16 can effectively improve the diagnostic efficiency of the disease.MSCT perfusion imaging of esophageal cancer lesions can indirectly reflect the angiogenesis of esophageal cancer, and the combination of CtBP2 and P16INK4A can effectively improve the diagnostic efficiency of the disease. Compared with colon cancer, the increase of morbidity is more significant for rectal cancer. The current study set out to identify novel and critical biomarkers or features that may be used as promising targets for early diagnosis and treatment monitoring of rectal cancer. Microarray datasets of rectal cancer with a minimum sample size of 30 and RNA-sequencing datasets of rectal adenocarcinoma (READ) were downloaded from the Gene Expression Omnibus (GEO) database and The Cancer Genome Atlas (TCGA) database. The method of robust rank aggregation was utilized to integrate differentially expressed genes (DEGs). The protein-protein interaction (PPI) network of the DEGs was structured using the STRING platform, and hub genes were identified using the Cytoscape plugin cytoHubba and an UpSet diagram. R software was employed to perform functional enrichment analysis. Receiver operating characteristic (ROC) curves based on the GEO data and Kaplan-Meier curves based on the TCGA data were drawn to assess the diagnostic and prognostic values of the hub genes.