Browse > Article
http://dx.doi.org/10.5483/BMBRep.2015.48.6.139

Apoptosis inhibitor 5 increases metastasis via Erk-mediated MMP expression  

Song, Kwon-Ho (Laboratory of Infection and Immunology, Graduate School of Medicine, Korea University)
Kim, Seok-Ho (Immunotherapy Research Center, Korea Research Institute of Bioscience & Biothechnology (KRIBB))
Noh, Kyung Hee (Laboratory of Infection and Immunology, Graduate School of Medicine, Korea University)
Bae, Hyun Cheol (Laboratory of Infection and Immunology, Graduate School of Medicine, Korea University)
Kim, Jin Hee (Laboratory of Infection and Immunology, Graduate School of Medicine, Korea University)
Lee, Hyo-Jung (Laboratory of Infection and Immunology, Graduate School of Medicine, Korea University)
Song, Jinhoi (Immunotherapy Research Center, Korea Research Institute of Bioscience & Biothechnology (KRIBB))
Kang, Tae Heung (Department of Immunology, School of Medicine, Konkuk University)
Kim, Dong-Wan (Department of Internal Medicine, Seoul National University College of Medicine)
Oh, Se-Jin (Laboratory of Infection and Immunology, Graduate School of Medicine, Korea University)
Jeon, Ju-Hong (Department of Physiology, Seoul National University, College of Medicine)
Kim, Tae Woo (Laboratory of Infection and Immunology, Graduate School of Medicine, Korea University)
Publication Information
BMB Reports / v.48, no.6, 2015 , pp. 330-335 More about this Journal
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. [BMB Reports 2015; 48(6): 330-335]
Keywords
Apoptosis inhibitor 5; Cervical cancer; Metastasis; Matrix metaloproteinase;
Citations & Related Records
연도 인용수 순위
  • Reference
1 Han BG, Kim KH, Lee SJ et al (2012) Helical repeat structure of apoptosis inhibitor 5 reveals protein-protein interaction modules. J Biol Chem 287, 10727-10737   DOI   ScienceOn
2 Rigou P, Piddubnyak V, Faye A et al (2009) The antiapoptotic protein AAC-11 interacts with and regulates Acinusmediated DNA fragmentation. EMBO J 28, 1576-1588   DOI   ScienceOn
3 Simon C, Simon M, Vucelic G et al (2001) The p38 SAPK pathway regulates the expression of the MMP-9 collagenase via AP-1-dependent promoter activation. Exp Cell Res 271, 344-355   DOI   ScienceOn
4 Wang Y and Prywes R (2000) Activation of the c-fos enhancer by the Erk MAP kinase pathway through two sequence elements: the c-fos AP-1 and p62TCF sites. Oncogene 19, 1379-1385   DOI
5 Gianfrancesco F, Esposito T, Ciccodicola A et al (1999) Molecular cloning and fine mapping of API5L1, a novel human gene strongly related to an antiapoptotic gene. Cytogenet Cell Genet 84, 164-166   DOI   ScienceOn
6 Morris L, Allen KE and La Thangue NB (2000) Regulation of E2F transcription by cyclin E-Cdk2 kinase mediated through p300/CBP co-activators. Nat Cell Biol 2, 232-239   DOI   ScienceOn
7 Morris EJ, Michaud WA, Ji JY, Moon NS, Rocco JW and Dyson NJ (2006) Functional identification of Api5 as a suppressor of E2F-dependent apoptosis in vivo. PLoS Genet 2, e196   DOI   ScienceOn
8 Tewari M, Yu M, Ross B, Dean C, Giordano A and Rubin R (1997) AAC-11, a novel cDNA that inhibits apoptosis after growth factor withdrawal. Cancer Res 57, 4063-4069
9 Koci L, Chlebova K, Hyzdalova M et al (2012) Apoptosis inhibitor 5 (API-5; AAC-11; FIF) is upregulated in human carcinomas in vivo. Oncology Lett 3, 913-916
10 Garcia-Jove Navarro M, Basset C, Arcondeguy T et al (2013) Api5 contributes to E2F1 control of the G1/S cell cycle phase transition. PLoS One 8, e71443   DOI
11 Ren K, Zhang W, Shi Y and Gong J (2010) Pim-2 activates API-5 to inhibit the apoptosis of hepatocellular carcinoma cells through NF-kappaB pathway. Pathol Oncol Res 16, 229-237   DOI
12 Van den Berghe L, Laurell H, Huez I, Zanibellato C, Prats H and Bugler B (2000) FIF [fibroblast growth factor-2 (FGF-2)-interacting-factor], a nuclear putatively antiapoptotic factor, interacts specifically with FGF-2. Mol Endocrinol 14, 1709-1724   DOI
13 Chung TW, Moon SK, Chang YC et al (2004) Novel and therapeutic effect of caffeic acid and caffeic acid phenyl ester on hepatocarcinoma cells: complete regression of hepatoma growth and metastasis by dual mechanism. FASEB J 18, 1670-1681   DOI   ScienceOn
14 Tseng HC, Lee IT, Lin CC et al (2013) IL-1beta promotes corneal epithelial cell migration by increasing MMP-9 expression through NF-kappaB- and AP-1-dependent pathways. PLoS One 8, e57955   DOI