胶质瘤已被证明是最恶性的颅内肿瘤之一，目前尚无有效的治疗方法。基于我们之前对氧化磷酸化（OXPHOS）抑制耐药和敏感癌细胞的RNA测序数据，我们发现VIM在OXPHOS抑制耐药的癌细胞中表达较高，特别是在胶质瘤癌细胞中。进一步研究发现，文献中对VIM的研究表明它在癌症进展、免疫治疗抑制、癌症干细胞性和药物耐药性方面起重要作用。然而，它在胶质瘤中的作用尚不明确。本研究旨在解析VIM在胶质瘤中的作用，特别是其在OXPHOS抑制敏感性方面的作用，这可能为胶质瘤治疗提供一个有前景的治疗靶点。我们从The Cancer Genome Atlas（TCGA）数据库获得了胶质瘤和正常组织中VIM的表达情况，并通过Human Protein Atlas（HPA）和Chinese Glioma Genome Atlas（CGGA）进行了进一步验证。单细胞测序数据来自TISCH2。通过Tumor Immune Estimation Resource（TIMER）、Estimation of Stromal and Immune Cells in Malignant Tumors using Expression Data（ESTIMATE）和ssGSEA计算了免疫渗入情况，通过R包计算了Immunophenoscore（IPS）。分析了VIM高表达组和低表达组之间的差异表达基因，包括GO/KEGG和Gene Set Enrichment Analysis（GSEA）。使用EWAS和Methsurv检查了VIM的甲基化情况。从SangerBox获得了VIM表达与肿瘤干细胞性之间的相关性。我们还使用了DepMap数据，在VIM高表达胶质瘤细胞中敲除VIM，以及在VIM低表达胶质瘤细胞中过表达VIM来检查细胞存活能力。与正常样本相比，Vim在胶质瘤患者中高表达，并且其高表达与患者生存率呈负相关。胶质瘤患者VIM启动子中的DNA甲基化低于正常样本。VIM高表达与免疫渗入和肿瘤进展呈正相关。此外，Vim在OXPHOS抑制胶质瘤癌细胞中高表达，在OXPHOS抑制敏感的癌细胞中低表达，并且其表达维持了OXPHOS抑制耐药性。总之，我们全面解析了VIM在胶质瘤进展及其临床预后中的作用，为结合当前治疗方法针对胶质瘤癌免疫治疗中的VIM提供了新的见解。© 2023. Springer Nature Switzerland AG.

Glioma has been demonstrated as one of the most malignant intracranial tumors and currently there is no effective treatment. Based on our previous RNA-sequencing data for oxidative phosphorylation (OXPHOS)-inhibition resistant and OXPHOS-inhibition sensitive cancer cells, we found that vimentin (VIM) is highly expressed in the OXPHOS-inhibition resistant cancer cells, especially in glioma cancer cells. Further study of VIM in the literature indicates that it plays important roles in cancer progression, immunotherapy suppression, cancer stemness and drug resistance. However, its role in glioma remains elusive. This study aims to decipher the role of VIM in glioma, especially its role in OXPHOS-inhibition sensitivity, which may provide a promising therapeutic target for glioma treatment.The expression of VIM in glioma and the normal tissue has been obtained from The Cancer Genome Atlas (TCGA) database, and further validated in Human Protein Atlas (HPA) and Chinese Glioma Genome Atlas (CGGA). And the single-cell sequencing data was obtained from TISCH2. The immune infiltration was calculated via Tumor Immune Estimation Resource (TIMER), Estimation of Stromal and Immune Cells in Malignant Tumors using Expression Data (ESTIMATE) and ssGSEA, and the Immunophenoscore (IPS) was calculated via R package. The differentiated expressed genes were analyzed including GO/KEGG and Gene Set Enrichment Analysis (GSEA) between the VIM-high and -low groups. The methylation of VIM was checked at the EWAS and Methsurv. The correlation between VIM expression and cancer stemness was obtained from SangerBox. We also employed DepMap data and verified the role of VIM by knocking down it in VIM-high glioma cell and over-expressing it in VIM-low glioma cells to check the cell viability.Vim is highly expressed in the glioma patients compared to normal samples and its high expression negatively correlates with patients' survival. The DNA methylation in VIM promoters in glioma patients is lower than that in the normal samples. High VIM expression positively correlates with the immune infiltration and tumor progression. Furthermore, Vim is expressed high in the OXPHOS-inhibition glioma cancer cells and low in the OXPHOS-inhibition sensitive ones and its expression maintains the OXPHOS-inhibition resistance.In conclusion, we comprehensively deciphered the role of VIM in the progression of glioma and its clinical outcomes. Thus provide new insights into targeting VIM in glioma cancer immunotherapy in combination with the current treatment.© 2023. Springer Nature Switzerland AG.