近日，PNAS發(fā)表了日本東京大學(xué)醫(yī)學(xué)研究所研究人員的一項(xiàng)新研究發(fā)現(xiàn),，對(duì)于癌癥發(fā)病和復(fù)發(fā)起到重要作用的癌干細(xì)胞,，能夠自己分泌其生存必需的各種蛋白質(zhì)。如果能夠破壞這個(gè)機(jī)制,，就有望防止癌癥的復(fù)發(fā),。
癌干細(xì)胞是指具有干細(xì)胞性質(zhì)的癌細(xì)胞，有“自我復(fù)制”以及“多細(xì)胞分化”等能力。這類(lèi)細(xì)胞被認(rèn)為有形成腫瘤乃至發(fā)展成癌癥的潛力?，F(xiàn)在的癌癥治療主要是通過(guò)藥物和放療等殺死癌細(xì)胞,。但是，如果有癌干細(xì)胞殘留,，癌細(xì)胞就會(huì)再次增殖,，而徹底殺死癌干細(xì)胞的技術(shù)一直沒(méi)有重大進(jìn)展。
研究人員從乳腺癌患者的癌組織中,，成功提取出癌干細(xì)胞,，研究發(fā)現(xiàn)，癌干細(xì)胞能夠自己分泌其生存所必需的各種物質(zhì),，包括細(xì)胞分裂和自我復(fù)制時(shí)需要的蛋白質(zhì)等,。
研究小組還發(fā)現(xiàn)，癌干細(xì)胞分泌的物質(zhì)還會(huì)進(jìn)入血液中,。研究人員說(shuō)，這一發(fā)現(xiàn)意味著可以通過(guò)血液檢查發(fā)現(xiàn)癌干細(xì)胞是否在增加,，從而有望對(duì)癌癥的發(fā)病和復(fù)發(fā)等進(jìn)行早期診斷,。（生物谷Bioon.com）
doi:10.1073/pnas.1113271109
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ErbB receptor tyrosine kinase/NF-κB signaling controls mammosphere formation in human breast cancer
Kunihiko Hinohara, Seiichiro Kobayashi, Hajime Kanauchi, Seiichiro Shimizu, Kotoe Nishioka, Ei-ichi Tsuji, Kei-ichiro Tada, Kazuo Umezawa, Masaki Mori, Toshihisa Ogawa, Jun-ichiro Inoue, Arinobu Tojo, and Noriko Gotoh
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.
