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Using shRNA to silence CD36 in LNCaP prostate cancer cells, the researchers found that treatment with SIM1-Me (10 nM) or ARV-110 (50 nM) led to: 5.6-fold and 19.6-fold reductions, respectively, in cellular drug uptake dramatically impaired target protein degradation markedly reduced cytotoxicity (up to 423-fold) Re-expression of CD36 restored activity, and loss of EEA1 also diminished SIM1-Me and ARV-110 cytotoxicity---confirming a dependence on the Rab5/EEA1 endocytic pathway

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