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Apoptosis inhibitor 5 increases metastasis via Erk-mediated MMP expression

Cited 12 time in Web of Science Cited 10 time in Scopus
Authors
Song, Kwon-Ho; Kim, Seok-Ho; Noh, Kyung Hee; Bae, Hyun Cheol; Kim, Jin Hee; Lee, Hyo-Jung; Song, Jinhoi; Kang, Tae Heung; Kim, Dong-Wan; Oh, Se-Jin; Jeon, Ju-Hong; Kim, Tae Woo
Issue Date
2015-06
Citation
BMB Reports, Vol.48 No.6, pp.330-335
Keywords
Apoptosis inhibitor 5Cervical cancerMetastasisMatrix metaloproteinase
Abstract
Apoptosis inhibitor 5 (API5) has recently been identified as a tumor metastasis-regulating gene in cervical cancer cells. However, the precise mechanism of action for API5 is poorly understood. Here, we show that API5 increases the metastatic capacity of cervical cancer cells in vitro and in vivo via up-regulation of MMP-9. Interestingly, API5-mediated metastasis was strongly dependent on the Erk signaling pathway. Conversely, knock-down of API5 via siRNA technology decreased the level of phospho-Erk, the activity of the MMPs, in vitro invasion, and in vivo pulmonary metastasis. Moreover, the Erk-mediated metastatic action was abolished by the mutation of leucine into arginine within the heptad leucine repeat region, which affects protein-protein interactions. Thus, API5 increases the metastatic capacity of tumor cells by up-regulating MMP levels via activation of the Erk signaling pathway.
ISSN
1976-6696
URI
http://hdl.handle.net/10371/165378
DOI
https://doi.org/10.5483/BMBRep.2015.48.6.139
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College of Medicine/School of Medicine (의과대학/대학원)Cancer Research Institute (암연구소)Journal Papers (저널논문_암연구소)
College of Medicine/School of Medicine (의과대학/대학원)Internal Medicine (내과학전공)Journal Papers (저널논문_내과학전공)
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