Apoptosis inhibitor 5 increases metastasis via Erk-mediated MMP expression

Kwon Ho Song, Seok Ho Kim, Kyung Hee Noh, Hyun Cheol Bae, Jin Hee Kim, Hyo Jung Lee, Jinhoi Song, Tae Heung Kang, Dong Wan Kim, Se Jin Oh, Ju Hong Jeon, Tae Woo Kim

Research output: Contribution to journalArticlepeer-review

15 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)330-335
Number of pages6
JournalBMB reports
Issue number6
Publication statusPublished - 2015


  • Apoptosis inhibitor 5
  • Cervical cancer
  • Matrix metaloproteinase
  • Metastasis

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology


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