Effects of miR-362 in Regulating the Proliferation, Invasion and Apoptosis of Gastric Cancer by Inhibiting the Expression of Tumor-Promoting Factor PRDM2.

Purpose - The high expression of positive regulatory domain zinc finger protein2 (PRDM2) is an important factor in inducing the formation and progression of gastric cancer. The current study was performed to explore the effect of micro-RNA-362 (miR-362) targeting PRDM2 on the proliferation and apoptosis of gastric cancer cells. Methods - The expression of miR-362 in gastric adenocarcinoma and normal gastric mucosa was detected by real-time fluorescence quantitative PCR (qPCR), and the expression of PRDM2 in gastric adenocarcinoma was detected by im-munohistochemical method. Gastric cancer cell line MGC-803 and human normal gastric mucosal epithelial cell line (GES-1) were selected for study. Blank control group, empty vector transfection group, miR-362 transfection group, and miR-362 and PRDM2 co-transfection group were established. CCK-8 assay was utilized to detect cell activity, flow cytometry was used to detect cell cycle and apoptosis, and invasion capability of cells was observed through transwell experiment. The expression of Cyclin D1 and Caspases-3 was detected by western blot method. Results - The expression of miR-362 in gastric adenocarcinoma was significantly lower than that in normal gastric mucosa. The expression of miR-362 in gastric adenocarcinoma was significantly different in the maximum diameter, depth of invasion, and different TNM stages. The expression of miR-362 was linked to prognosis. In addition, there was a negative correlation between miR-362 and PRDM2. The expression of miR-362 in gastric cancer cell line MGC-803 was significantly lower than that in GES-1. Compared with the blank control group and empty vector transfection group, the proliferation level of gastric cancer cells in miR-362 transfection group was remarkably decreased, the cells in S phase and G2/M phase were significantly decreased, the capability for invasion was evidently decreased, while the apoptosis was significantly increased. The expression of Caspases-3 increased significantly and the expression of Cyclin D1 decreased significantly. MiR-362 and PRDM2 co-transfection groups could reverse the abovementioned expression levels. Conclusion - MiR-362 can regulate the proliferation, invasion and apoptosis of gastric cancer by inhibiting the expression of tumor-promoting factor PRDM2. The expression of miR-362 in gastric adenocarcinoma is significantly decreased, which can regulate the formation and development of gastric adenocarcinoma by promoting the expression of PRDM2. Moreover, low expression of miR-362 in gastric adenocarcinoma is an important risk factor for tumor progression and poor prognosis.

Pan-cancer analysis reveals correlation between RAB3B expression and tumor heterogeneity, immune microenvironment, and prognosis in multiple cancers.

RAB3B is essential for the transportation and secretion within cells. Its increased expression is linked to the development and progression of various malignancies. However, understanding of RAB3B's involvement in carcinogenesis is mostly limited to specific cancer subtypes. Hence, exploring RAB3B's regulatory roles and molecular mechanisms through comprehensive cancer datasets might offer innovative approaches for managing clinical cancer. To examine the potential involvement of RAB3B in the development of cancer, we analyzed data from various sources including The Cancer Genome Atlas (TCGA), Genotype-Tissue Expression Project (GTEx), cBioPortal, HPA, UALCAN, and tissue microarray (TAM). Using bioinformatics techniques, we examined the correlation between RAB3B expression and prognosis, tumor heterogeneity, methylation modifications, and immune microenvironment across different cancer types. Our findings indicate that elevated RAB3B expression can independently predict prognosis in many tumors and has moderate accuracy for diagnosing most cancers. In most cancer types, we identified RAB3B mutations that showed a significant correlation with tumor mutational burden (TMB), mutant-allele tumor heterogeneity (MATH), and microsatellite instability (MSI). Abnormal DNA methylation patterns were also observed in most cancers compared to normal tissues. Additionally, we found significant correlations between RAB3B expression, immune cell infiltration, and immune scores across various cancers. Through pan-cancer analysis, we observed significant differences in RAB3B expression levels between tumors and normal tissues, making it a potential primary factor for cancer diagnosis and prognosis. The IHC results revealed that the expression of RAB3B in six types of tumors was consistent with the results of the pan-cancer analysis of the database. Furthermore, RAB3B showed potential associations with tumor heterogeneity and immunity. Thus, RAB3B can be utilized as an auxiliary diagnostic marker for early tumor detection and a prognostic biomarker for various tumor types.

Situs Inversus Totalis on 18F-FDG PET/CT: A Case Report and a Literature Review.

A 62-year-old female patient with pathologically confirmed left lung small cell neuroendocrine carcinoma. The patient was referred to our positron emission tomography (PET)/CT center to look for possible metastatic diseases. After fasting for 8 h, the fasting blood glucose level of the patient was 7.1 mmol/L. The patient was intravenously injected with a 6.42 mCi (238 MBq) 18F-fluorodeoxyglucose (FDG) imaging agent. After the patient rested for 1 h, we scanned the patient with SIEMENS Biograph mCT 64 PET/CT camera. In addition to lung tumors and lymph node diseases, abnormal tracer uptake in the patient's thyroid was also found. PET/CT also showed situs inversus totalis of the patient, including the dextrocardia, liver on the left side, stomach, and spleen on the right side of the patient's body. The identification of anatomical variations and abnormalities by PET/CT imaging is very important to develop the best treatment for lung cancer.

Comprehensive Analysis of Hexokinase 2 Immune Infiltrates and m6A Related Genes in Human Esophageal Carcinoma.

Background: Hexokinase 2 not only plays a role in physiological function of human normal tissues and organs, but also plays a vital role in the process of glycolysis of tumor cells. However, there are few comprehensive studies on HK2 in esophageal carcinoma (ESCA) needs further study. Methods: Oncomine, Tumor Immune Estimation Resource (TIMER), The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) database were used to analyze the expression differences of HK2 in Pan-cancer and ESCA cohort, and to analyze the correlation between HK2 expression level and clinicopathological features of TCGA ESCA samples. GO/KEGG, GGI, and PPI analysis of HK2 was performed using R software, LinkedOmics, GeneMANIA and STRING online tools. The correlation between HK2 and ESCA immune infiltration was analyzed TIMER and TCGA ESCA cohort. The correlation between HK2 expression level and m6A modification of ESCA was analyzed by utilizing TCGA ESCA cohort. Results: HK2 is highly expressed in a variety of tumors, and its high expression level in ESCA is closely related to the weight, cancer stages, tumor histology and tumor grade of ESCA. The analysis results of GO/KEGG showed that HK2 was closely related to cell adhesion molecule binding, cell-cell junction, ameboidal-type cell migration, insulin signaling pathway, hif-1 signaling pathway, and insulin resistance. GGI showed that HK2 associated genes were mainly involved in the glycolytic pathway. PPI showed that HK2 was closely related to HK1, GPI, and HK3, all of which played an important role in tumor proliferation. The analysis results of TIMER and TCGA ESCA cohort indicated that the HK2 expression level was related to the infiltration of various immune cells. TCGA ESCA cohort analyze indicated that the HK2 expression level was correlated with m6A modification genes. Conclusion: HK2 is associated with tumor immune infiltration and m6A modification of ESCA, and can be used as a potential biological target for diagnosis and therapy of ESCA.