Home FOR AUTHORS Neoplasma 2013 Neoplasma Vol.60, No.5, p.493-503, 2013

Journal info


6 times a year.
Founded: 1954
ISSN 0028-2685
ISSN 1338-4317 (online)

Published in English

Editorial Info
Abstracted and Indexed
Submission Guidelines

Select Journal







Webshop Cart

Your Cart is currently empty.

Info: Your browser does not accept cookies. To put products into your cart and purchase them you need to enable cookies.

Neoplasma Vol.60, No.5, p.493-503, 2013

Title: p21-activated kinase 4 regulation of endometrial cancer cell migration and invasion involves the ERK1/2 pathway mediated MMP-2 secretion
Author: W. Lu, Y. H. Xia, J. J. Qu, Y. Y. He, B. L. Li, C. Lu, X. Luo, X. P. Wan

Abstract: Endometrial cancer (EC) is one of the most common malignancy of the female genital tract. Patients with metastatic disease have a poor prognosis. So far, however, the underlying molecular mechanisms of EC metastasis are largely unknown. P21-activated kinase 4 (Pak4) is important in cell motility and oncogenesis. Here we investigated a role of Pak4 in EC cell migration and invasion. Pak4 overexpression was observed in multiple human EC cell lines. In clinical samples, expression of total and phosphorylated Pak4 (Pak4 and p-Pak4, respectively) increased significantly with progression of EC from normal tissue to lymph node metastasis; both were positively correlated with depth of myometrial and vascular space invasion, lymph nodes metastasis, and poor histological differentiation. In two human EC cell lines, Pak4 overexpression promoted cell migration and invasion in vitro. Short hairpin RNA (shRNA)-mediated stable knockdown of Pak4 inhibited the metastatic potential of EC in an ERK1/2-MMP-2-dependent manner. These results suggest that Pak4 is an important regulator of EC cell migration and invasion. Therefore, Pak4 may be a promising target for the treatment of metastatic EC.

Keywords: p21-activated kinase 4 (Pak4); endometrial cancer (EC); metastasis; migration; invasion; ERK1/2; MMP-2
Published online: 24-Jun-2013
Year: 2013, Volume: 60, Issue: 5 Page From: 493, Page To: 503
doi:10.4149/neo_2013_064


download file



© AEPress s.r.o
Copyright notice: For any permission to reproduce, archive or otherwise use the documents in the ELiS, please contact AEP.