Activin signal promotes cancer progression and is involved in cachexia in a subset of pancreatic cancer

Yosuke Togashi, Akihiro Kogita, Hiroki Sakamoto, Hidetoshi Hayashi, Masato Terashima, Marco A. de Velasco, Kazuko Sakai, Yoshihiko Fujita, Shuta Tomida, Masayuki Kitano, Kiyotaka Okuno, Masatoshi Kudo, Kazuto Nishio

Research output: Contribution to journalArticlepeer-review

63 Citations (Scopus)


We previously reported that activin produces a signal with a tumor suppressive role in pancreatic cancer (PC). Here, the association between plasma activin A and survival in patients with advanced PC was investigated. Contrary to our expectations, however, patients with high plasma activin A levels had a significantly shorter survival period than those with low levels (median survival, 314 days vs. 482 days, P=0.034). The cellular growth of the MIA PaCa-2 cell line was greatly enhanced by activin A via non-SMAD pathways. The cellular growth and colony formation of an INHBA (beta subunit of inhibin)-overexpressed cell line were also enhanced. In a xenograft study, INHBA-overexpressed cells tended to result in a larger tumor volume, compared with a control. The bodyweights of mice inoculated with INHBA-overexpressed cells decreased dramatically, and these mice all died at an early stage, suggesting the occurrence of activin-induced cachexia. Our findings indicated that the activin signal can promote cancer progression in a subset of PC and might be involved in cachexia. The activin signal might be a novel target for the treatment of PC.

Original languageEnglish
Pages (from-to)819-827
Number of pages9
JournalCancer Letters
Issue number2
Publication statusPublished - Jan 28 2015
Externally publishedYes


  • Activin signal
  • Cachexia
  • Pancreatic cancer

ASJC Scopus subject areas

  • Oncology
  • Cancer Research


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