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P300 promotes migration, invasion and epithelial-mesenchymal transition in a
nasopharyngeal carcinoma cell line
#MMPMID28356956
Liao ZW
; Zhao L
; Cai MY
; Xi M
; He LR
; Yu F
; Zhou TC
; Liu MZ
Oncol Lett
2017[Feb]; 13
(2
): 763-769
PMID28356956
show ga
A previous study demonstrated that p300 is overexpressed in nasopharyngeal
carcinoma (NPC), and that its expression is an independent prognostic factor. The
aim of the present study is to investigate the role of p300 in human NPC
development. A small hairpin (sh) RNA lentiviral expression vector targeting the
p300 gene was constructed to suppress the expression of p300 in NPC cells.
Knockdown of p300 was verified by reverse transcription-quantitative polymerase
chain reaction and western blotting. Wound-healing, invasion, immunofluorescence
and immunoprecipitation assays were performed to assess the influence of p300 on
nasopharyngeal tumorigenesis and metastasis in vitro. The expression of p300 was
upregulated in NPC cell lines. After knockdown of p300, the migration and
invasion ability of shp300 cells were significantly inhibited (P<0.05).
Furthermore, the depletion of p300 expression in NPC cell lines resulted in the
upregulation of epithelial phenotype marker E-cadherin and ?-catenin, and
downregulation of mesenchymal phenotype markers N-cadherin and vimentin. p300
promotes epithelial-mesenchymal transition (EMT) through the acetylation of Smad2
and Smad3 in the tumor growth factor-? signaling pathway. In conclusion, p300 may
be involved in the invasion and metastasis of NPC through the induction of EMT.
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