前列腺癌是众所周知依赖雄激素受体（AR）进行生长和存活的，因此AR是治疗该疾病的主要药理学靶点。然而，在最初对AR靶向治疗的积极响应后，前列腺癌最终会进化为去势抗性前列腺癌，这往往是致命的。最初认为肿瘤生长会在治疗后变得雄激素非依赖性; 但是，分子研究的结果表明，大多数耐药机制都涉及AR的重新激活。因此，肿瘤细胞变得对去势 - 阻止睾酮产生的睾丸雄激素 - 而不是对AR本身独立。然而，如何正确定义前列腺癌的临床前模型（包括细胞系）仍存在困惑。大多数细胞系是在肿瘤进化为去势抗性前列腺癌后，从患者中分离用于细胞培养的，但并非所有这些细胞系都描述为去势抗性。此外，去势是指睾丸通过阻断睾酮产生; 因此，即使是体外的“去势”概念也是有问题的。为确保从科学研究到临床的知识最大限度地转移，了解临床前模型的限制和优势，以及这些模型如何重复癌细胞的雄激素依赖性并可用于研究去势耐药机制是至关重要的。© 2023年 Springer Nature Limited。

Prostate cancer is well known to be dependent on the androgen receptor (AR) for growth and survival. Thus, AR is the main pharmacological target to treat this disease. However, after an initially positive response to AR-targeting therapies, prostate cancer will eventually evolve to castration-resistant prostate cancer, which is often lethal. Tumour growth was initially thought to become androgen-independent following treatments; however, results from molecular studies have shown that most resistance mechanisms involve the reactivation of AR. Consequently, tumour cells become resistant to castration - the blockade of testicular androgens - and not independent of AR per se. However, confusion still remains on how to properly define preclinical models of prostate cancer, including cell lines. Most cell lines were isolated from patients for cell culture after evolution of the tumour to castration-resistant prostate cancer, but not all of these cell lines are described as castration resistant. Moreover, castration refers to the blockade of testosterone production by the testes; thus, even the concept of "castration" in vitro is questionable. To ensure maximal transfer of knowledge from scientific research to the clinic, understanding the limitations and advantages of preclinical models, as well as how these models recapitulate cancer cell androgen dependency and can be used to study castration resistance mechanisms, is essential.© 2023. Springer Nature Limited.