z-logo
Premium
Anti‐proliferative Effect of Kv1.3 in A549 Human Lung Adenocarcinoma in vitro and in vivo
Author(s) -
Jang Soo Hwa,
Choi Sun Young,
Ryu DougYoung,
Ryu Pan Dong,
Lee So Yeong
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.lb649
Subject(s) - a549 cell , in vivo , adenocarcinoma , cancer research , cell growth , small hairpin rna , in vitro , chemistry , cell cycle , potassium channel , cyclin , cell , microbiology and biotechnology , apoptosis , cancer , biology , medicine , endocrinology , gene knockdown , biochemistry
Voltage‐gated potassium channels (Kv) are widely expressed in the plasma membranes of numerous cells and contribute to a variety of cellular functions in both excitable neuronal cells and non‐excitable epithelial cells. Recently, it has been demonstrated that Kv channels are associated with the proliferation of several types of cancer cells. In the present study, we investigated the effects of suppressed expression of Kv1.3 on cell proliferation and cell cycle distribution in human lung adenocarcinoma, A549 cells. Treatment with margatoxin (MgTX), a selective blocker of Kv1.3, and shRNA against Kv1.3, significantly blocked A549 cell proliferation. In addition, selective inhibition of Kv1.3 significantly increased expression level of p21 Waf1/Cip1 and significantly decreased the expression level of Cdk4 and cyclin D3. We also applied the MgTX into a xenograft model using nude mice and MgTX caused a reduction of tumor volume when it was injected into tumor tissues. These results suggest that Kv1.3 may serve as a novel therapeutic target for lung adenocarcinoma therapy. This work is supported by National Research Foundation of Korea (2009‐0066580)

This content is not available in your region!

Continue researching here.

Having issues? You can contact us here