BackgroundTripartite motif-containing protein 28 (TRIM28) is a transcriptional corepressor involved in the regulation of several cancers, including glioma. It has been reported that TRIM28 takes part in the process of autophagy. However, its effect on the autophagy and cell proliferation in gliomas has not been elucidated. Here, we report a novel tumor cell proliferation mechanism in which TRIM28-regulated autophagy promotes glioma tumor cell proliferation.Materials and methodsWe analyzed the expressions of TRIM28 and LC3 in different WHO grades of gliomas by IHC assays. We then knocked down and overexpressed TRIM28 or knocked down ATG5 in U251 cells and confirmed its roles in autophagy and cell proliferation via cell counting, immunofluorescence, and Western blot.ResultsThe results showed that TRIM28 and autophagy levels were significantly increased with the progression of tumor grade in glioma. TRIM28 promoted glioblastoma cell proliferation. Knockdown of TRIM28 inhibited autophagy in glioblastoma cells. Meanwhile, TRIM28 promoted glioblastoma cell proliferation by modulating TRIM28.ConclusionThese data demonstrated that TRIM28 activates autophagy and increases cell proliferation in glioma.

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Background: CXCR (CXC Chemokine Receptor) is a complex of the immune-associated protein involved in tumor activation, invasion, migration, and angiogenesis through various chemical signals in the tumor microenvironment (TME). However, significant prognostic characteristics of CXCR members and their impact on the occurrence and progression of glioma have not yet been fully elucidated.Methods: In this research, we used Oncomine, TCGA, GTEx, and CGGA databases to analyze the transcription and survival data of glioma patients. Afterward, the influence of CXCR members on the TME was explored using comprehensive bioinformatics analysis.Results: The mRNA expression levels of CXCR1/2/3/4/7 were significantly up-regulated in glioma than in normal samples, whereas the mRNA expression level of CXCR5 was decreased. We then summarized the genetic alteration landscape of CXCR and identified two molecular subtypes based on CXCR expression patterns in glioma. The characteristics of CXCRs were also investigated, including the clinicopathological parameters, TME cell infiltration, and prognosis of patients with glioma. After Lasso and multivariable Cox regression, a CR-Score for predicting overall survival (OS) was constructed and the predictive performance of the signature was validated. The high-risk group was a significantly poorer prognostic group than the low-risk group as judged by the CR-Score (TCGA cohort, p < 0.001, CGGA cohort, p < 0.001). Moreover, the CR-Score was significantly correlated to the tumor-immune infiltration and cancer stem cell (CSC) index. A risk scale-based nomogram incorporating clinical factors for individual risk estimation was established thereby.Conclusion: These findings may pave the way for enhancing our understanding of CXCR modification patterns and developing better immune therapeutic approaches for glioma.