There have been several studies that have linked elevated scavenger receptor class b type 1 (SR-B1) expression and activity to the development and progression of castration-resistant prostate cancer (CRPC). SR-B1 facilitates the influx of cholesterol to the cell from lipoproteins in systemic circulation. This influx of cholesterol may be important for many cellular functions, including the synthesis of androgens. Castration-resistant prostate cancer tumors can synthesize androgens de novo to supplement the loss of exogenous sources often induced by androgen deprivation therapy. Silencing of SR-B1 may impact the ability of prostate cancer cells, particularly those of the castration-resistant state, to maintain the intracellular supply of androgens by removing a supply of cholesterol. SR-B1 expression is elevated in CRPC models and has been linked to poor survival of patients. The overarching belief has been that cholesterol modulation, through either synthesis or uptake inhibition, will impact essential signaling processes, impeding the proliferation of prostate cancer. The reduction in cellular cholesterol availability can impede prostate cancer proliferation through both decreased steroid synthesis and steroid-independent mechanisms, providing a potential therapeutic target for the treatment of prostate cancer. In this article, we discuss and highlight the work on SR-B1 as a potential novel drug target for CRPC management.

中文翻译：

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抑制清道夫受体 B 类 1 型 (SR-B1) 表达和活性作为破坏去势抵抗性前列腺癌中胆固醇可用性的潜在新靶标

有几项研究将清道夫受体 B 类 1 型 (SR-B1) 表达和活性升高与去势抵抗性前列腺癌 (CRPC) 的发展和进展联系起来。SR-B1 促进胆固醇从体循环中的脂蛋白流入细胞。这种胆固醇的流入可能对许多细胞功能很重要，包括雄激素的合成。去势抵抗性前列腺癌肿瘤可以从头合成雄激素，以补充通常由雄激素剥夺疗法引起的外源性来源的损失。SR-B1 的沉默可能会影响前列腺癌细胞的能力，特别是那些去势抵抗状态的细胞，通过去除胆固醇的供应来维持细胞内雄激素的供应。SR-B1 表达在 CRPC 模型中升高，并与患者的不良生存率有关。首要的信念是胆固醇调节，通过合成或摄取抑制，将影响基本的信号传导过程，阻碍前列腺癌的增殖。细胞胆固醇可用性的降低可以通过减少类固醇合成和类固醇独立机制来阻碍前列腺癌的增殖，为前列腺癌的治疗提供潜在的治疗靶点。在本文中，我们讨论并强调了 SR-B1 作为 CRPC 管理的潜在新药靶点的工作。阻止前列腺癌的扩散。细胞胆固醇可用性的降低可以通过减少类固醇合成和类固醇独立机制来阻碍前列腺癌的增殖，为前列腺癌的治疗提供潜在的治疗靶点。在本文中，我们讨论并强调了 SR-B1 作为 CRPC 管理的潜在新药靶点的工作。阻止前列腺癌的扩散。细胞胆固醇可用性的降低可以通过减少类固醇合成和类固醇独立机制来阻碍前列腺癌的增殖，为前列腺癌的治疗提供潜在的治疗靶点。在本文中，我们讨论并强调了 SR-B1 作为 CRPC 管理的潜在新药靶点的工作。