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Next Generation Sequencing Facilitates Quantitative Analysis of U87 Transcriptomes to define the ALKBH5-dependent hypoxia-induced genes

ABSTRACT: Among 720 hypoxia-induced genes (at least 2 folds of upregulation in Hypoxia-treated U87 WT or shScr cells compared with Normoxia), the expression of 35 genes is significantly suppressed by ALKBH5 depletion (U87 Hypoxia shALKBH5/shScr)

ORGANISM(S): Homo sapiens

PROVIDER: GSE171227 | GEO | 2024/03/31

REPOSITORIES: GEO

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Project description:Purpose: Hypoxia is a predominant feature in GBM and its microenvironment. It is associated with the tumor growth, progression and resistance to conventional therapy of GBM. We have utilized U87-MG cell line as a human GBM cell model and human brain HEB cell line as non-neoplastic brain cell cultured in different levels of hypoxia for transcriptional profiling to identify the transcriptional signature of U87-MG cells for elucidated the role of hypoxia in GBM phenotype. Methods: We have utilized U87-MG cell line as a human GBM cell model and human brain HEB cell line as non-neoplastic brain cell cultured in 21%, 5% and 1% O2 for 24h. Then we detected the changes of transcriptional profiling and analyzed the biological process and pathway for the genes with different expression modes in different hypoxia levels. Results: U87-MG cells present specific transcriptional signature response to different hypoxia levels. The genes associated with organ and system development present an upward trend from normoxia to extreme hypoxia. And the biological process of DNA repair presents a downward trend, indicating that gene mutations of U87-MG cells could derive by hypoxia microenvironment. Otherwise, HEB cells present the canonical response to hypoxia, reducing of the metabolic rate in concert with the degree of hypoxia and extracting more oxygen from the environment. Conclusion: Hypoxia microenvironment could promote the malignance of GBM through activate of genes involved in organ and system development. Meanwhile it could induce the mutations of genes in GBM, especially extreme hypoxia.

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