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The AKR1C3/AR‐V7 complex maintains CRPC tumour growth by repressing B4GALT1 expression
Multiple mechanisms contribute to the survival and growth of metastatic castration‐resistant prostate cancer (mCRPC) cells without androgen, including androgen receptor splice variants (AR‐V) and de novo intratumoral androgen synthesis. AKR1C3 is a critical androgenic enzyme that plays different rol...
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| 出版年: | J Cell Mol Med |
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| 主要な著者: | , , , , , , , , |
| フォーマット: | Artigo |
| 言語: | Inglês |
| 出版事項: |
John Wiley and Sons Inc.
2020
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| 主題: | |
| オンライン･アクセス: | https://ncbi.nlm.nih.gov/pmc/articles/PMC7579719/ https://ncbi.nlm.nih.gov/pubmed/32902124 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1111/jcmm.15831 |
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