Research press release


Nature Medicine

Targeting the stem of cancer



John Dickたちは、多くの遺伝子の発現に影響するマウスタンパク質BMI-1が、幹細胞の自己再生や腫瘍形成に不可欠な因子であることを、ヒトの結腸直腸がん細胞系列や結腸直腸がん患者由来の細胞試料で突き止めた。Dickたちは、BMI-1レベルを低下させる化合物を開発した。この化合物は、がん幹細胞の機能を阻害し、マウスにおける一次ヒト結腸直腸がんの成長を妨げた。これらの結果が示すように、BMI-1の阻害という戦略を使えば、がんの治療を改善し、抗腫瘍効果を持続させられる可能性がある。

A therapeutic drug strategy against colorectal cancer stem cells in mice is reported this week in Nature Medicine. As cancer stem cells are considered to be one of the reasons for the cause of therapy resistance and tumor relapse, this approach could be further developed for more effective cancer treatments.

Cancers are composed of various cell populations, including a small but recalcitrant stem cell fraction that can replenish itself and also give rise to more differentiated tumor cells. The elimination of the cancer stem cell population is considered necessary to achieve complete cancer eradication; however, these stem cells have unique properties that make them resistant to many cancer therapies, and so far they have proven to be elusive targets.

John Dick and colleagues identify a mouse protein BMI-1, a protein that can affect the expression of genes, as a crucial factor for stem cell self-renewal and tumor formation in human colorectal cell lines and colorectal tumor patient samples. The authors develop a compound that diminishes BMI-1 levels and therefore impairs cancer stem function and growth of primary human colorectal cancers in mice. These results suggest that BMI-1 inhibition could be used to improve cancer therapy and provide lasting anti-tumor effects.

doi: 10.1038/nm.3418


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