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UBE2C induces EMT through Wnt/??catenin and PI3K/Akt signaling pathways by
regulating phosphorylation levels of Aurora-A
#MMPMID28260026
Wang R
; Song Y
; Liu X
; Wang Q
; Wang Y
; Li L
; Kang C
; Zhang Q
Int J Oncol
2017[Apr]; 50
(4
): 1116-1126
PMID28260026
show ga
The ubiquitin-conjugating enzyme 2C (UBE2C) is the key component in the ubiquitin
proteasome system (UPS) by partnering with the anaphase?promoting
complex (APC/C). A high UBE2C protein expression level has been reported in
various types of human tumors. However, little is known about the precise
mechanism by which UBE2C expression is downregulated in gastric cancer. We found
in MGC?803 and SGC?7901 gastric cancer cells UBE2C?deficient G2/M phase arrest in
the cell cycle and subsequently decreased gastric adenocarcinoma tumorigenesis.
In the previous study, we identified Aurora-A (AURKA) as the hub gene of the
gastric cancer linkage network based genome?wide association study (eGWAS).
Furthermore, knockdown of UBE2C using siRNA markedly reduced the level of
phosphorylation AURKA (p?AURKA) via Wnt/??catenin and PI3K/Akt signaling pathways
suppressed the occurrence and development of gastric cancer. Additionally, the
expression of E?cadherin was up?regulated and N-cadherin was downregulated in
response to UBE2C knockdown and inhibits epithelial-mesenchymal transition (EMT).
Collectively, our data suggest that the activity of AURKA might be regulated by
UBE2C through regulating the activity of APC/C. UBE2C may be a new marker in the
diagnosis of gastric cancer and may be a potential therapeutic target for the
treatment of gastric adenocarcinoma.
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