Research press release


Nature Medicine

Taming prostate cancer aggressiveness



R Reiterたちは、性腺摘除抵抗性の前立腺がんでは、細胞間で糊の働きをするタンパク質N-カドヘリンの発現が上昇していることを発見した。男性ホルモン依存性前立腺がんでN-カドヘリンを発現させると、がんは性腺摘除抵抗性になり、転移が促進された。N-カドヘリンに対するモノクローナル抗体は、マウスに移植した前立腺がんの増殖、接着、転移を抑制し、一部の例では腫瘍が完全に退縮した。

The cell-adhesion molecule N-cadherin is critical for the tumour transition from a relatively benign to a very aggressive form of prostate cancer, reports an article published online this week in Nature Medicine. Therapeutic targeting of this adhesion molecule may have future clinical benefits for the treatment of prostate cancer.

Men with prostate cancer tend to respond to castration therapy, as prostate tumours are often dependent on androgenic hormones to grow. If, on the other hand, the tumour becomes androgen-independent and resistant to castration, the disease becomes lethal. What controls the transition to the castration-resistant state has been unknown.

Robert Reiter and his colleagues found that the expression of N-cadherin, a protein that acts as molecular glue between cells, is increased in tumours of people with castration-resistant prostate cancer. They found that forced expression of N-cadherin in androgen-dependent prostate cancer cells made them resistant to castration and promoted cancer metastasis. Monoclonal antibodies against N-cadherin reduced proliferation, adhesion and metastasis of prostate cancer cells transplanted into mice, leading in some cases to complete tumour regression.

doi: 10.1038/nm.2236


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