Research press release




転移は、がん関連死の主たる原因だが、ほとんどのがんについて、転移の引き金となる細胞が同定されておらず、そのために転移抑制治療の開発が難題となっている。今回、Salvador Aznar Benitahの研究グループは、ヒトの口腔がん検体に含まれる細胞型が脂肪酸受容体CD36を高発現し、マウスにおける転移能が高いことを明らかにした。そしてマウスのがんモデルを用いた実験で抗体を使ってCD36を遮断したところ、転移が有意に減少し、既存の転移巣が明らかに縮小あるいは消失した。


The discovery of a specific metastasis-promoting cell type has led to the development of a drug that can, in mouse models, prevent the spread of cancer from one body part to another. The findings, reported online in Nature this week, also highlight a prominent role for dietary lipids in cancer metastasis.

Metastasis is the main cause of cancer-related death, but for most cancers, the identity of the cells that trigger the phenomenon is unknown. This makes the development of anti-metastatic therapies difficult. Salvador Aznar Benitah and colleagues have identified a cell type, found in human oral carcinoma samples, that expresses high levels of the fatty acid receptor, CD36, and that has high metastatic potential in mice. When the receptor is blocked using antibodies in mouse cancer models, metastasis is significantly reduced, and metastases that are already present notably shrink or disappear.

The antibody has a metastasis-blocking effect, not just for human oral carcinoma cells injected into mouse cancer models, but also for human melanoma and breast cancer cells. This finding suggests there may be a general mechanism underlying tumour metastasis, and hints that CD36-blocking therapies might have widespread application. Clinically, the presence of these CD36-expressing cells correlates with poor prognosis for many different carcinomas, and in mouse models, a high fat diet appears to boost the cells’ metastatic potential.

doi: 10.1038/nature20791

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