前列腺癌是男性癌症死亡的第五大原因，2020年造成超过375,000人死亡。需要开发新的治疗策略以改善预后。大麻植物中的化学成分——大麻素，可能是一种可行的解决方案。临床前证据显示，大麻素能够调节多种肿瘤类型的多个癌症特征。然而，大麻素在前列腺癌中的治疗潜力尚未完全探索。本研究旨在研究体外条件下大麻二酚（CBD）对前列腺癌细胞的抗增殖和抗侵袭性能。CBD抑制了细胞的存活能力和增殖，并伴随着关键细胞周期蛋白（具体是D3环蛋白、CDK2、CDK4和CDK1）的表达下调以及AKT磷酸化的抑制。CBD对细胞存活能力的影响未受大麻素受体拮抗剂、瞬时受体电位热痛素1（TRPV1）通道阻断剂或G蛋白偶联受体GPR55激动剂的阻断，这表明CBD在前列腺癌细胞中的作用独立于这些靶点。此外，CBD减少了高度转移性PC-3细胞的侵袭性，并增加了E-钙黏蛋白的蛋白表达。CBD抑制前列腺癌细胞增殖和侵袭能力的能力表明CBD可能具有未来作为化疗药物的潜力。

Prostate cancer is the fifth leading cause of cancer death in men, responsible for over 375,000 deaths in 2020. Novel therapeutic strategies are needed to improve outcomes. Cannabinoids, chemical components of the cannabis plant, are a possible solution. Preclinical evidence demonstrates that cannabinoids can modulate several cancer hallmarks of many tumor types. However, the therapeutic potential of cannabinoids in prostate cancer has not yet been fully explored. The aim of this study was to investigate the antiproliferative and anti-invasive properties of cannabidiol (CBD) in prostate cancer cells in vitro. CBD inhibited cell viability and proliferation, accompanied by reduced expression of key cell cycle proteins, specifically cyclin D3 and cyclin-dependent kinases CDK2, CDK4, and CDK1, and inhibition of AKT phosphorylation. The effects of CBD on cell viability were not blocked by cannabinoid receptor antagonists, a transient receptor potential vanilloid 1 (TRPV1) channel blocker, or an agonist of the G-protein-coupled receptor GPR55, suggesting that CBD acts independently of these targets in prostate cancer cells. Furthermore, CBD reduced the invasiveness of highly metastatic PC-3 cells and increased protein expression of E-cadherin. The ability of CBD to inhibit prostate cancer cell proliferation and invasiveness suggests that CBD may have potential as a future chemotherapeutic agent.