Identification of Family with Sequence Similarity 110 Member C (FAM110C) as a Candidate Diagnostic and Prognostic Biomarker for Glioma.

Background: Gliomas are the most frequent and dangerous primary cerebral tumors. Therefore, there is a need to develop molecular targets for the diagnosis and treatment for glioma. Methods: In September 2020, we retrieved the expression matrix of glioblastoma (GBM) sufferers and pertinent clinical data from the TCGA (The Cancer Genome Atlas) database. Prognostic differences between various families with sequence similarity 110 member C (FAM110C) expression groups were assessed by Kaplan-Meier with log-rank test. The R platform get used to assess the accuracy of FAM110C delivery in predicting the prognosis of PDAC using a time-dependent receptor operating characteristic (ROC) curve. The delivery level of FAM110C was determined by qRT-PCR and western blot. Gene set enrichment investigated possible mechanisms between different FAM110C expression groups in GBM (GSEA). The impact of FAM110C on glioma cell movement was discovered using migration test. The drug's gene-targeting impact was validated by the CCK8 test. Results: A total of 173 GBM samples were obtained from the TCGA database, with 148 including information on IDH1 mutations and 151 containing information on overall survival. The mRNA expression level of FAM110C was greater in wild-type GBM, according to qRT-PCR data. The connection between FAM110C expression and Hallmark, GO, and KEGG pathway gene sets was investigated using GSEA software. We used migration test to assess the impact of FAM110C on glioma motility in order to confirm the findings of the GSEA analysis. Conclusion: FAM110C might get used as a possible diagnostic and prognostic biomarker for wild-type GBM, and its inhibition could be used to prevention and treatment wild-type GBM.

FAM84B promotes the proliferation of glioma cells through the cell cycle pathways.

BACKGROUND: This study aimed to investigate FAM84B expression in glioma tissues and explore the role of FAM84B in promoting the proliferation of glioma cells and the mechanism of regulating the cell cycle pathways. METHODS: The TCGA database was adopted to analyze FAM84B expression in glioma tissues. The FAM84B expression was detected by qRT-PCR in patients with glioma, especially that in glioma cells, U251, LN-229, U98, and U87. Two glioma cell lines U87 and T98 were selected for siRNA transfection, which were divided into si-NC si-FAM84B-1 and si-FAM84B-2 groups. The effect of FAM84B on the proliferation of glioma cells was detected with the MTT experiment and that on the glioma cell cycle was detected with the flow cytometry. The signaling pathways potentially regulated by FAM84B in glioma were analyzed through the bioinformatics analysis. The expression of proteins, Cyclin D1, CDK4, Cdk6, and p21, in the cell cycle-related pathways in cells of each group was detected by the Western blot. RESULTS: TCGA database results showed a significantly higher FAM84B expression in glioma tissues than that in paracancerous tissues. According to the detection of qRT-PCR, FAM84B expressed the highest in the glioma cell line U87 (P < 0.05). Compared with the serum of healthy controls, FAM84B mRNA expression significantly increased in patients with gliomas. And compared with the si-NC group, the proliferation ability of U87 and T98 cells decreased and the cell cycle was blocked in the G0/G1 phase in both si-FAM84B transfection groups (P < 0.05). According to the bioinformatics analysis, FAM84B regulated the cell cycle pathways in glioma. FAM84B siRNA inhibited the expression of key proteins, Cyclin D1, CDK2, CDK4, and Cdk6, of the cell cycle pathways in glioma cells and promoted the expression of P53 and P21 proteins. CONCLUSIONS: In conclusion, FAM84B may inhibit the proliferation of glioma cells by regulating the cell cycle pathways.

Circ-EZH2 knockdown reverses DDAH1 and CBX3-mediated cell growth and invasion in glioma through miR-1265 sponge activity.

Accumulating evidence has indicated the important roles of circular RNAs (circRNAs) in different tumors. However, their detailed regulatory mechanisms in glioma are not fully understood. In this study, the functional role of a novel circRNA, circ-EZH2, was investigated by cell counting kit-8 (CCK-8), colony formation, flow cytometry, and transwell experiments. The regulatory mechanism of circ-EZH2 was explored by bioinformatics analysis, quantitative real-time PCR (qRT-PCR), Western blot and dual-luciferase reporter assay. We identified that circ-EZH2 was overexpressed in glioma tissues and cell lines. Further studies revealed that ectopic expression of circ-EZH2 significantly promoted cell growth, migration and invasion but inhibited cell apoptosis. By contrast, silencing of circ-EZH2 induced the opposite effects. Additionally, we found circ-EZH2 served as a miRNA sponge for miR-1265 to release its suppression on DDAH1 and CBX3. Rescue assays further revealed that the oncogenic function of circ-EZH2 was partly dependent on its modulation of DDAH1 and CBX3. Our study unraveled a novel molecular pathway in glioma and may provide a new perspective for the treatment of glioma.