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JST Press Release

Oct.1, 2012

Japan Science and Technology Agency (JST)
5-3, Yonbancho, Chiyoda-ku, Tokyo 102-8666

Identifying the mechanism of cancer progression by cell-cell communication

Mitochondrial function is frequently impaired in human cancers; however, the mechanism by which mitochondrial defect contributes to tumor growth and progression is not known. Using the Drosophila genetic mosaic technique, Igaki and colleagues found that defects in mitochondrial function cooperate with oncogenic Ras activation to induce tumor progression and metastasis of surrounding benign tumors through the secretion of Unpaired (an IL-6 homolog) and Wingless (a Wnt homolog).

Researcher Information

JST PRESTO Research Area “Elucidation and control of the mechanisms underlying chronic inflammation”

Research Theme : “Molecular basis of non-genetic tumor progression driven by epithelial oncogenic inflammation”

Journal Information

Published on 30 September 2012 as Advance Online Publication in “Nature”.
Shizue Ohsawa, Yoshitaka Sato, Masato Enomoto, Mai Nakamura, Aya Betsumiya & Tatsushi Igaki
“Mitochondrial defect drives non-autonomous tumour progression through Hippo signalling in Drosophila”

doi: 10.1038/nature11452


[About Research]
Tatsushi Igaki Ph.D.
Associate Professor, Kobe University Graduate School of Medicine,

[About Program]

Tetsuya Ishii,
Life Innovation Group, Department of Innovation Research, Japan Science and Technology Agency


JST, an integrated organization of science and technology in Japan, establishes an infrastructure for the entire process from the creation of knowledge to the return to the society. For more information, visit http://www.jst.go.jp/EN/