ArticleScientific reports2014
Overexpression of DCF1 inhibits glioma through destruction of mitochondria and activation of apoptosis pathway.
Article in Scientific reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- Microsomal glutathione transferase 1 in cancer and the regulation of ferroptosis.Advances in cancer research · 2023Review
- Interactions between microglia and glioma in tumor microenvironment.Frontiers in oncology · 2023Review
- Dcf1 induces glioblastoma cells apoptosis by blocking autophagy.Cancer medicine · 2022Article
- TMEM59 interacts with TREM2 and modulates TREM2-dependent microglial activities.Cell death & disease · 2020Article
- Whole slide images reflect DNA methylation patterns of human tumors.NPJ genomic medicine · 2020Article
- Dendritic cell factor 1 inhibits proliferation and migration and induces apoptosis of neuroblastoma cells by inhibiting the ERK signaling pathway.Oncology reports · 2019Article
- TMEM59 potentiates Wnt signaling by promoting signalosome formation.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Article
- A novel multikinase inhibitor R8 exhibits potent inhibition on cancer cells through both apoptosis and autophagic cell death.Oncotarget · 2017Article
- Dynamin-related protein 1 controls the migration and neuronal differentiation of subventricular zone-derived neural progenitor cells.Scientific reports · 2015Article
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gliomas are the most common brain tumors affecting the central nervous system and are associated with a high mortality rate. DCF1 is a membrane protein that was previously found to play a role in neural stem cell differentiation. In the present study, we found that overexpression of dcf1 significantly inhibited cell proliferation, migration, and invasion and dramatically promoted apoptosis in the glioblastoma U251 cell line. DCF1 deletion mutations in the functional region showed that the complete structure of DCF1 was necessary for apoptosis. Furthermore, significantly lower tumorigenicity was observed in athymic nude mice by transplanting U251 cells overexpressing dcf1. To decode the apoptosis induced by dcf1, mitochondrial structure and membrane potential in glioma cells were investigated and the results indicated obvious mitochondrial swelling, destruction of cristae, and a significant decline in membrane potential. Mechanismly, caspase-3 signaling was activated. Finally, endogenous dcf1 silence in U251 cells was investigated. Results showed a highly methylation at -1339 and -1322 position at dcf1 promoter sequence, revealing the causal relationship between dcf1 gene and tumorigencicity. The present study identified a previously unknown cancer apoptosis mechanism involving dcf1 overexpression and provided a novel approach to potentially treat glioma patients.
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