ArticleInternational journal of clinical and experimental pathology2018
CD300A inhibits tumor cell growth by downregulating AKT phosphorylation in human glioblastoma multiforme.
Article in International journal of clinical and experimental pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed, 3 citations in OpenAlex.
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma multiforme (GBM) is a primary malignant tumor of the central nervous system with the highest incidence and dismal prognosis. As a member of the CD300 glycoprotein family, CD300A plays a role in cell proliferation, apoptosis, differentiation, and immune response, but its role in solid tumors remains unknown. In this study, CD300A was observed to be overexpressed in human GBM samples using real-time PCR and western blotting. To investigate the role of CD300A in GBM, CCK8, transwell and flow cytometry analysis were performed to examine the proliferation, migration and apoptosis in GBM cell lines, respectively. From our results, knockdown of CD300A blocks cell proliferation and migration, and induces cell apoptosis in human GBM cells U251MG and U87MG. Further, we assessed AKT expression level in CD300A knockdown and negative control cells. The phosphorylation level of AKT was significantly suppressed in CD300A knockdown cells in comparison to negative control cells, suggesting that CD300A promoted tumor cell growth through the AKT pathway. In conclusion, our findings expand the knowledge of CD300A as an oncogene in solid tumor, and provide experimental and theoretical basis for further clinical application.
Indexed as
Identifiers
31949725PMC6962892W3007362972What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.