Guo S.,Mudanjiang Medical University |
Guo S.,Key Laboratory of Cancer Prevention and Treatment of Heilongjiang Province |
Yu L.,Harbin Medical University |
Cheng Y.,Mudanjiang Medical University |
And 16 more authors.
Cell Biology International | Year: 2012
We have examined the effects of bFGF (basic fibroblast growth factor) on p-ERK (phosphorylated extracellular signalregulated kinase) through PDGFRβ (platelet-derived growth factor receptor β) in the proliferation and migration of EPCs (endothelial progenitor cells). EPC migration was detected using the Transwell system. The expression of PDGFRβ mRNA and protein, total ERK and p-ERK proteins was respectively assessed by real-time PCR and Western blottings. bFGF promote the proliferation and migration of EPCs, the effects of bFGF being implemented by activating ERK signalling through the expression of PDGFRβ, whereas an anti-bFGF antibody and inhibitor of PDGF (platelet-derived growth factor) receptor kinase (AG1296) could respectively decrease the expression of PDGFRβ mRNA and protein and p-ERK protein. Total ERK protein did not change under the same experimental conditions, and an inhibitor of p-ERK (PD98059) inhibited the proliferation and migration of EPCs. The findings strongly suggest that a PDGFRβ/p-ERK signalling pathway triggered by bFGF plays an important role in the proliferation and migration of EPCs. © The Author(s) Journal compilation © 2012 International Federation for Cell Biology.
An J.,Key Laboratory of Cancer Prevention and Treatment of Heilongjiang Province |
An J.,Mudanjiang Medical University |
Zhu X.,Key Laboratory of Cancer Prevention and Treatment of Heilongjiang Province |
Wang H.,Mudanjiang Medical University |
Jin X.,Key Laboratory of Cancer Prevention and Treatment of Heilongjiang Province
International Journal of Oncology | Year: 2013
Alternative polyadenylation and microRNA regulation are both mechanisms of post-transcriptional regulation of gene expression. Alternative polyadenylation often results in mRNA isoforms with the same coding sequence but different lengths of 3' UTRs, while microRNAs regulate gene expression by binding to specific mRNA 3' UTRs. In this sense, different isoforms of an mRNA may be differentially regulated by microRNAs, sometimes resulting in cellular proliferation and this mechanism is being speculated on as a potential cause for cancer development.