ITGB4 upregulation is associated with progression of lower grade glioma
Gliomas originating in the neuroepithelium account for about 80% of brain malignancies and are the most common cancer of the central nervous system. Clinical management of gliomas remains challenging despite significant advances in comprehensive therapies, including radiotherapy, chemotherapy, and s...
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Veröffentlicht in: | Scientific reports 2024-01, Vol.14 (1), p.421-421, Article 421 |
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Zusammenfassung: | Gliomas originating in the neuroepithelium account for about 80% of brain malignancies and are the most common cancer of the central nervous system. Clinical management of gliomas remains challenging despite significant advances in comprehensive therapies, including radiotherapy, chemotherapy, and surgery. The
ITGB4
(Integrin subunit beta 4) gene encodes a receptor for laminins and its upregulation in tumor tissues is associated with poor prognosis. However, its role in glioma is not well understood. First, we performed a pan cancer analysis of
ITGB4
expression in The Cancer Genome Atlas (TCGA) dataset. Survival analysis was done on Chinese Glioma Genome Atlas (CGGA) and TCGA. Immunohistochemistry was then used to validate the expression and role of
ITGB4
in glioma. We finally analyzed the possible mechanism by immune infiltration and single-cell sequencing analysis. Here, we found that
ITGB4
is upregulated in glioma and accurately predicts the prognosis of lower grade glioma (LGG). Univariate and multivariate Cox regression analyses showed that
ITGB4
is a risk factor for LGG. Immunohistochemical analysis confirmed that
ITGB4
accurately predicts LGG prognosis. Non-negative matrix factorization (NMF) cluster analysis showed that
ITGB4
was closely related to immune related genes. Immune cell infiltration and single cell sequencing analyses indicated that
ITGB4
may be closely related to the microenvironment of gliomas, especially tumor-associated fibroblasts.
ITGB4
is a promising diagnostic and therapeutic factor in LGG patients. |
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ISSN: | 2045-2322 2045-2322 |
DOI: | 10.1038/s41598-023-49801-y |