PBF, a Proto-oncogene in Esophageal Carcinoma.
AKT/mTOR
PBF
Wnt3a/β-catenin
apoptosis
proliferation
Journal
Open medicine (Warsaw, Poland)
ISSN: 2391-5463
Titre abrégé: Open Med (Wars)
Pays: Poland
ID NLM: 101672167
Informations de publication
Date de publication:
2019
2019
Historique:
received:
18
11
2018
accepted:
26
07
2019
entrez:
23
10
2019
pubmed:
23
10
2019
medline:
23
10
2019
Statut:
epublish
Résumé
Emerging evidence shows that the pituitary tumour-transforming gene (PTTG)-binding factor (PBF) functions as a proto-oncogene in some tumors. However, the precise functions of PBF in tumorigenesis and its action mechanisms remain largely unknown. Here for the first time we demonstrated that PBF was associated with a tumor-related cell phenotype in esophageal carcinoma (ESCA) and identified the involved signaling pathways. PBF was up-regulated in ESCA tissues (Data from GEPIA) and cells. Then we down-regulated PBF in ESCA cell lines, Eca-109 and TE-1, by using RNAi technology. Cell function analysis suggested that down-regulation of PBF could inhibit tumor-related cell phenotypes, including proliferation, motility, apoptosis and cell cycle, in Eca-109 and TE-1 cells. Mechanism investigation suggested that apoptosis induced by PBF knockdown may be mediated by the activation of the mitochondrial apoptosis pathway and cell cycle arrest. AKT/mTOR and Wnt3a/β-catenin, key pathways in regulating tumor proliferation and metastasis, were found to be inactivated by the down-regulation of PBF in ESCA cells. In conclusion, our study demonstrates that PBF functions as a proto-oncogene in ESCA in vitro, which may be mediated through AKT/mTOR and Wnt3a/β-catenin pathways.
Identifiants
pubmed: 31637306
doi: 10.1515/med-2019-0086
pii: med-2019-0086
pmc: PMC6795029
doi:
Types de publication
Journal Article
Langues
eng
Pagination
748-756Informations de copyright
© 2019 Shi-hai Lian et al., published by De Gruyter.
Déclaration de conflit d'intérêts
Conflict of interest: Authors state no conflict of interest.
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