


Although the incident and pathological background have been described, the detailed mechanisms of the extracellular environment are still unknown.Ĭollagen is a polypeptide that accounts for approximately one-third of the extracellular matrix (ECM) protein of connective tissue in the human body. These events include the IDH1 R132 mutation, CpG island methylator phenotype (CIMP) status, methylation state of MGMT, ATRX loss-of-function mutations, EGFR amplification, and several chromosomal abnormalities (chromosome 1p-19q codeletion, chromosome 7 gain-of-function and chromosome 10 loss-of-function). They defined the proneural, classical and mesenchymal subtypes and multiple corresponding events. In recent years, scientists have tried to classify the subtypes and genetic alterations. Temozolomide (TMZ) is the only chemotherapeutic drug that has been approved by the US Food and Drug Administration (FDA) for the treatment of GBM. At present, the treatment for brain cancer mainly includes surgery, chemotherapy, radiation therapy, immunotherapy, etc. The other type is primary tumor lesions derived from glial cells, which account for half of all brain tumors and are almost all malignant tumors. In addition, brain tumors are the most common metastatic tumors, mainly metastasizing from the lung, breast and urinary system. According to the World Health Organization (WHO), Gliomas are divided into low-grade (grades II and III) (Low grade glioma, LGG) and high-grade (grade IV) (GBM). Glioblastoma (GBM) is a common malignant glioma in the brain and is aggressive. Our results indicate that the COL5A1−PPRC1−ESM1 axis may represent a novel therapeutic target in GBM. We investigated the involvement of COL5A1 in extracellular remodeling and the regulation of actin filaments in the metastasis of GBM. Moreover, PPRC1, GK and ESM1 were predicted by ingenuity pathway analysis (IPA) to be transcription factors or to participate downstream. Based on these results, we established a transcriptomics dataset based on COL5A1. Most importantly, we validated the cell mobility, metastatic ability and actin polymerization status caused by COL5A1 with two-way models. In addition, our cohort also showed a consistent trend in COL5A1 protein levels. We further examined whether the overexpression of COL5A1 is common in mesenchymal subtypes and is related to the survival rate of GBM patients through several in silico cohorts. Therefore, we screened various collagen types and observed that the type V collagen α1 chain (COL5A1) gene plays a pivotal role in GBM.

Previous studies have shown that the collagen family is involved in the regulation of the extracellular environment of cancer cells, and these conditions could become an important factor for effective treatment. Existing therapies do not have significant efficacy for GBM patients.
