NF-κB non-cell-autonomously regulates cancer stem cell populations in the basal-like breast cancer subtype

Mizuki Yamamoto, Yuu Taguchi, Taku Ito-Kureha, Kentaro Semba, Noritaka Yamaguchi and Jun-ichiro Inoue ()
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Mizuki Yamamoto: Institute of Medical Science, University of Tokyo, Shirokane-dai, Minato-ku, Tokyo 108-8639, Japan
Yuu Taguchi: Institute of Medical Science, University of Tokyo, Shirokane-dai, Minato-ku, Tokyo 108-8639, Japan
Taku Ito-Kureha: Cell Signal Unit, Okinawa Institute of Science and Technology Graduate University, Onna-son, Kunigami-gun, Okinawa 904-0495, Japan
Kentaro Semba: Waseda University, Wakamatsu-cho, Shinjuku-ku, Tokyo 162-8480, Japan
Noritaka Yamaguchi: Graduate School of Pharmaceutical Sciences, Chiba University
Jun-ichiro Inoue: Institute of Medical Science, University of Tokyo, Shirokane-dai, Minato-ku, Tokyo 108-8639, Japan

Nature Communications, 2013, vol. 4, issue 1, 1-13

Abstract: Abstract Patients with triple-negative breast cancer display the highest rates of early relapse of all patients with breast cancer. The basal-like subtype, a subgroup of triple-negative breast cancer, exhibits high levels of constitutively active NF-κB signalling. Here we show that NF-κB activation, induced by inflammatory cytokines or by epigenetically dysregulated NIK expression, cell-autonomously upregulates JAG1 expression in non-cancer stem cells. This upregulation stimulates NOTCH signalling in cancer stem cells in trans, leading to an expansion of cancer stem cell populations. Among breast cancers, the NF-κB-dependent induction of JAG1 and the NOTCH-dependent expansion of the cancer stem cell population occur only in the basal-like subtype. Collectively, our results indicate that NF-κB has a non-cell-autonomous role in regulating cancer stem cell populations by forming intratumoural microenvironments composed of JAG1-expressing non-cancer stem cells with a basal-like subtype.

Date: 2013
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DOI: 10.1038/ncomms3299

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