Distinct responses of patient-derived GBM cell lines to hypoxia
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ABSTRACT:
PROVIDER: PRJNA973646 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24622879.fastq.gz | Fastqsanger.gz | |||
| SRR24622880.fastq.gz | Fastqsanger.gz | |||
| SRR24622881.fastq.gz | Fastqsanger.gz | |||
| SRR24622882.fastq.gz | Fastqsanger.gz | |||
| SRR24622883.fastq.gz | Fastqsanger.gz |
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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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Project description:Glioblastoma (GBM) presents a formidable clinical challenge due to its complex microenvironment. Here, we introduce tumor-associated foam cells (TAFs), a previously unidentified immune cell entity of lipid droplet (LD)-loaded macrophages, in GBM. Through extensive analyses of patient tumors, together with in vitro and in vivo investigations, we reveal that TAFs exhibit distinct pro-tumorigenic characteristics related to hypoxia, mesenchymal transition, angiogenesis, and impaired phagocytosis. Moreover, TAF presence correlates with worse patient outcome. Our mechanistic investigations demonstrate that TAF formation is facilitated by lipid cargo transfer from extracellular vesicles released by GBM cells. Importantly, we demonstrate that targeting key enzymes involved in LD formation, such as DGAT1 or ACSL, effectively disrupts TAF functionality. This study establishes TAFs as a prominent immune cell entity in GBM and provides valuable insights into their interplay within the microenvironment. Disrupting LD formation to target TAFs presents an interesting avenue for future therapeutic development in GBM.
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