ArticleNPJ precision oncology2024
COL8A1 overexpression promotes glioma cell growth by activating focal adhesion kinase signaling cascade.
Article in NPJ precision oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- Multi-omics profiling-derived signature links cellular ecosystem to glioblastoma prognosis.iScience · 2026Article
- Mitochondrial complex I subunit NDUFS4 overexpression drives glioma progression by regulating mitochondrial function and COX5B.NPJ precision oncology · 2026Article
- Wnt signalling facilitates neuronal differentiation of cochlear Frizzled10-positive cells in mouse cochlea via glypican 6 modulation.Cell communication and signaling : CCS · 2025Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We explored expression and biological roles of collagen type VIII alpha-1 chain (COL8A1) in glioma. Bioinformatics analyses unveiled COL8A1 overexpression within glioma tissues correlates with adverse clinical outcomes of patients. COL8A1 overexpression was also detected in local glioma tissues and various glioma cells. In primary and immortalized glioma cells, COL8A1 shRNA or knockout (KO) reduced cell viability, proliferation and mobility, disrupted cell cycle, and prompted apoptosis. While COL8A1 overexpression augmented the malignant behaviors in glioma cells. COL8A1 shRNA or KO in primary glioma cells decreased phosphorylation of FAK and downstream targets Akt and Erk1/2. Conversely, elevating COL8A1 expression increased their phosphorylations. In vivo experiments confirmed growth inhibition of patient-derived glioma xenografts within the mouse brain following COL8A1 KO. Hindered proliferation, lowered phosphorylation levels of FAK, Akt, and Erk1/2, as well as increased apoptosis were observed within the COL8A1 KO intracranial glioma xenografts. Thus, COL8A1 overexpression promotes glioma cell growth.
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Registered trials
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