Glioma is one of the most common tumors in the brain and complete cure still a challenge. The present research aimed to investigate the molecular mechanism of circular RNA SMO (circSMO742) in glioma, via targeting miR-338-3p and regulating SMO expression. QRT-PCR was utilized to examine the expression profiles of circSMO742 and microRNA-338-3p (miR-338-3p) in glioma. SMO protein in glioma was tested via western blot. RNA pulldown assay and dual luciferase reporter assays were used to explore the targeting correlation between RNAs. MTT assay, transwell assays and flow cytometry were used to investigate cell proliferation, migration and invasion, and apoptosis, respectively. Tumor xenograft was done to ascertain the effect of circSMO742 knocking down on tumor growth. CircSMO742 and SMO were highly expressed in glioma tissues, while miR-338-3p expression was reduced. CircSMO742 together with SMO could promote cells proliferation, migration and invasion while inhibit cells apoptosis, whereas miR-338-3p showed negative impacts on the cell activity. Knocking down of circSMO742 suppressed glioma growing in vivo. CircSMO742 promoted glioma growth by sponging miR-338-3p to regulate SMO expression. Our research revealed a new molecular mechanism of glioma growth and provide a fresh perspective on circRNAs in glioma progression.
Background: PYD and CARD domain-containing (PYCARD) was upregulated in TMZ-resistant cell lines and glioma tissue and was correlated with poor prognosis, its role in glioma is unclear known. The aim of this study was to elucidate the relationship between PYCARD and glioma based on Gene Expression Omnibus (GEO), The Cancer Genome Atlas (TCGA), and Chinese Glioma Genome Atlas (CGGA) databases.Methods: Glioma-resistant cells were compared with parental cells based on the GSE53014 and GSE113510 data sets. The relationship between PYCARD, tumor microenvironment, and long noncoding RNAs (lncRNAs) was assessed using logistic regression. Moreover, Kaplan-Meier and Cox regression were used to analyze the relationship between PYCARD expression and survival rate. Gene set enrichment analysis (GSEA) was also used to determine the biological function of PYCARD and lncRNAs. Cell viability and cell migration assays were used to evaluate the ability of cells to migrate and proliferate. Finally, we analyzed the expression patterns of PYCARD genes in a wide range of cancers.Results: Elevated expression of PYCARD promoted glioma cell proliferation and migration. PYCARD expression was significantly positively associated with gamma delta T cells but negatively correlated with M2 macrophages in glioblastoma multiforme (GBM). Likewise, PYCARD expression was significantly positively associated with monocytes but negatively associated with activated mast cells in low grade glioma (LGG).We also found that 3 PYCARD-related lncRNAs in GBM and 4 PYCARD-related lncRNAs in LGG had a predictive value for glioma patients. The pan-cancer analysis showed that PYCARD expression was higher in most cancer groups.Conclusions: High expression of PYCARD is an independent predictor of unfavorable prognosis and chemotherapy resistance in glioma.
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