{'fraction_non_alphanumeric': 0.022972972972972974, 'fraction_numerical': 0.0, 'mean_word_length': 6.484848484848484, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Prostate cancer cells survive anti‐androgen and mitochondrial metabolic inhibitors by modulating glycolysis and mitochondrial metabolic activities

Most cancer cells are more glycolytic even under aerobic conditions compared with their normal counterparts. Recent evidence of tumor cell metabolism, however, shows that some tumors also increase mitochondrial oxidative phosphorylation (ox‐phos) at some disease states during progression and/or development of drug resistance. Our data show that anti‐androgen enzalutamide (ENZA) resistant prostate cancer (PCa) cells use more mitochondrial metabolism leading to higher ox‐phos as compared to the ENZA‐sensitive cells and can become vulnerable to mitochondrial metabolism targeted therapies.