The Role of RNA Methylation Modification Related Genes in Prognosis and Immunotherapy of Colorectal Cancer.

Background: Researches showed RNA methylation genes can affect the prognosis of tumors. Thus, the study aimed to comprehensively analyze the effects of RNA methylation regulatory genes in prognosis and treatment of colorectal cancer (CRC).

Methods: Prognostic signature associated with CRCs were constructed by differential expression analysis, Cox and Least Absolute Shrinkage and Selection Operator (LASSO) analyses.

Hsa_circ_0079480 enhances cell proliferation, migration, and invasion in colorectal cancer through miR-498/ATP5E axis.

Circular RNAs play critical roles in tumorigenesis. hsa_circ_0079480 was reported to be upregulated in colorectal cancer (CRC). However, its specific molecule in CRC is poorly understood.

Inhibitory Effects of in Esophageal Squamous Cell Carcinoma: Network Pharmacology and Experimental Validation.

Esophageal squamous cell carcinoma (ESCC) is one of the most frequently occurring diseases in the world. (RR) has been demonstrated to be effective against ESCC; however, the mechanism is unknown. The primary gene modules related to the clinical characteristics of ESCC were initially investigated in this research using weighted gene co-expression network analysis (WCGNA) and differential expression gene (DEG) analysis.

The function of Sphingosine-1-phosphate receptor 2 (S1PR2) in maintaining intestinal barrier and inducing ulcerative colitis.

Sphingosine-1-phosphate receptor 2 (S1PR2) was highly expressed in intestinal epithelial cells (IECs) and facilitated the proliferation of IECs. However, the specific function of S1PR2 in intestinal diseases, such as ulcerative colitis (UC), remains unclear. Accordingly, the current study set out to investigate the function of S1PR2 in maintaining intestinal barrier and inducing UC.

The Sphingosine-1-Phosphate/Sphingosine-1-Phosphate Receptor 2 Axis in Intestinal Epithelial Cells Regulates Intestinal Barrier Function During Intestinal Epithelial Cells-CD4+T-Cell Interactions.

Background/aims: Epithelial cells line the intestinal mucosa and form an important barrier for maintaining host health. This study aimed to explore the mechanism of the Sphingosine-1-phosphate (S1P)/Sphingosine-1-phosphate receptor 2 (S1PR2) pathway in intestinal epithelial cells (IECs) that participate in the intestinal barrier function.

Methods: In this study, we constructed a knockout of the S1PR2 gene in mice, and Dextra sulfate sodium (DSS) was used to induce colitis.

MiR-126 impairs the intestinal barrier function via inhibiting S1PR2 mediated activation of PI3K/AKT signaling pathway.

Background: Aberrant expression of miRNAs was a critical element in the pathogenesis of inflammatory bowel disease (IBD). This study aimed to explore the involvement and mechanism of miR-126 in IBD.

Methods: In this study, the endogenous expressions of miR-126, S1PR2 and S1P in the pathological tissues of patients with IBD were detected using qRT-PCR and western blot assay, respectively.

MiR-34c and PlncRNA1 mediated the function of intestinal epithelial barrier by regulating tight junction proteins in inflammatory bowel disease.

Background: Inflammatory bowel disease (IBD) is originated from uncontrolled inflammation, and desired methods for IBD therapy remains the main difficult. The network comprised with miRNA and lncRNA has been verified to play an important role on diverse human diseases. In this study, we demonstrated the role of miR-34c and lncRNA PlncRNA1 on the function of intestinal barrier.

Abdominal lymphangiomatosis in a 38-year-old female: case report and literature review.

Lymphangioma is an uncommon benign tumor that develops in the lymphatic system. Abdominal lymphangiomatosis is extremely rare in adult patients, and the clinical symptoms of this condition are complicated and atypical. We report a case of abdominal lymphangiomatosis in a 38-year-old female who presented with intestinal bleeding and protein-losing enteropathy, as well as lesions in the lung and bones.