CLEC5A promotes the proliferation of gastric cancer cells by activating the PI3K/AKT/mTOR pathway.
Biochem Biophys Res Commun
; 524(3): 656-662, 2020 04 09.
Article
em En
| MEDLINE
| ID: mdl-32033754
ABSTRACT
Gastric cancer (GC), as one of the most prevalent malignancies, contributes to the high morbidity and mortality worldwide. By analyzing the bioinformatics, qRT-PCR and IHC assays, we found that CLEC5A is overexpressed in GC and associated with poorer prognosis. CLEC5A silencing inhibits cell growth and DNA replication and induces cell cycle arrest and cell apoptosis. Bioinformatics analyses and Western blotting revealed that CLEC5A depletion led to the dysregulation of the PI3K/AKT/mTOR pathway. CLEC5A-mediated GC proliferation and anti-apoptosis were impaired by blocking the PI3K/AKT/mTOR pathway with LY294002. We hypothesize that CLEC5A is of vital importance to GC initiation and progression via the PI3K/AKT/mTOR pathway, and that our results might represent promising therapeutic strategies for GC patients.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Neoplasias Gástricas
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Receptores de Superfície Celular
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Fosfatidilinositol 3-Quinases
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Lectinas Tipo C
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Proteínas Proto-Oncogênicas c-akt
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Serina-Treonina Quinases TOR
Limite:
Humans
Idioma:
En
Revista:
Biochem Biophys Res Commun
Ano de publicação:
2020
Tipo de documento:
Article