Division of Systems Biomedical Technology, Institute of Medical Science, University of Tokyo, Minato-ku, Tokyo 108-8639, Japan.
Proc Natl Acad Sci U S A. 2012 Apr 24;109(17):6584-9. doi: 10.1073/pnas.1113271109. Epub 2012 Apr 5.
Breast cancer is one of the most common cancers in humans. However, our understanding of the cellular and molecular mechanisms underlying tumorigenesis in breast tissues is limited. Here, we identified a molecular mechanism that controls the ability of breast cancer cells to form multicellular spheroids (mammospheres). We found that heregulin (HRG), a ligand for ErbB3, induced mammosphere formation of a breast cancer stem cell (BCSC)-enriched population as well as in breast cancer cell lines. HRG-induced mammosphere formation was reduced by treatment with inhibitors for phosphatidyl inositol 3-kinase (PI3K) or NF-κB and by expression of IκBα-Super Repressor (IκBαSR), a dominant-negative inhibitor for NF-κB. Moreover, the overexpression of IκBαSR in breast cancer cells inhibited tumorigenesis in NOD/SCID mice. Furthermore, we found that the expression of IL8, a regulator of self-renewal in BCSC-enriched populations, was induced by HRG through the activation of the PI3K/NF-κB pathway. These findings illustrate that HRG/ErbB3 signaling appears to maintain mammosphere formation through a PI3K/NF-κB pathway in human breast cancer.
乳腺癌是人类最常见的癌症之一。然而,我们对于乳腺组织中肿瘤发生的细胞和分子机制的理解还很有限。在这里,我们发现了一个控制乳腺癌细胞形成多细胞球体(类乳腺球体)能力的分子机制。我们发现,表皮生长因子受体 3(ErbB3)的配体,即人表皮生长因子样神经生长因子(heregulin,HRG),可以诱导富含乳腺癌干细胞(breast cancer stem cell,BCSC)的群体以及乳腺癌细胞系形成类乳腺球体。PI3K 或 NF-κB 的抑制剂处理以及 IκBα-Super Repressor(IκBαSR)的表达(NF-κB 的显性负抑制剂)降低了 HRG 诱导的类乳腺球体形成。此外,乳腺癌细胞中 IκBαSR 的过表达抑制了 NOD/SCID 小鼠的肿瘤发生。此外,我们发现 HRG 通过激活 PI3K/NF-κB 通路诱导了富含 BCSC 群体中自我更新调节剂 IL8 的表达。这些发现表明,HRG/ErbB3 信号似乎通过 PI3K/NF-κB 通路在人乳腺癌中维持类乳腺球体的形成。