PO.TB10.17 · 肿瘤生物学
维生素D（骨化三醇）增强前列腺癌细胞系中CB2介导的抗肿瘤反应：分子机制与治疗潜力
Vitamin D (calcitriol) potentiates CB2-mediated anti-tumor responses in prostate cancer cell lines: Molecular mechanisms and therapeutic potential
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摘要 Abstract
中文摘要
前列腺癌（PCa）是美国男性中最常被诊断的非皮肤癌，并仍是癌症相关死亡的第二大原因。维生素D受体（VDR）信号在前列腺肿瘤中发挥抗增殖和促分化作用，而大麻素受体2（CB2）则被认为参与免疫调节和抗肿瘤活性。新出现的证据提示CB2激活与VDR通路之间可能存在交互作用。我们假设CB2激活可诱导前列腺癌细胞中VDR的表达。将DU145和PC3细胞在完全RPMI培养基中铺板24小时，血清饥饿24小时，然后用10 nM骨化三醇、1 nM AM1241（CB2激动剂）或单独饥饿培养基处理。在PC3细胞中，AM1241诱导VDR表达的水平与骨化三醇相当，而DU145细胞相对于对照仅显示极微弱的诱导。这些初步发现提示存在细胞系依赖性效应，即CB2激动作用可能增强VDR表达。正在进行的研究正评估CB2激活是否进一步增强VDR信号传导并调节其在前列腺癌中的肿瘤抑制功能。
查看英文原文 English abstract
Prostate cancer (PCa) is the most frequently diagnosed non-skin cancer among U.S. men and remains the second leading cause of cancer-related mortality. Vitamin D receptor (VDR) signaling exerts antiproliferative and pro-differentiation effects in prostate tumors, while Cannabinoid Receptor 2 (CB2) has been implicated in immune modulation and antitumor activity. Emerging evidence suggests potential crosstalk between CB2 activation and VDR pathways. We hypothesize that CB2 activation induces VDR expression in prostate cancer cells. DU145 and PC3 cells were plated in complete RPMI for 24 hours, serum-starved for 24 hours, and treated with 10 nM calcitriol, 1 nM AM1241 (CB2 agonist), or starvation media alone. In PC3 cells, AM1241 induced VDR expression at levels comparable to calcitriol, whereas DU145 cells showed minimal induction relative to controls. These preliminary findings suggest a cell line-dependent effect whereby CB2 agonism may enhance VDR expression. Ongoing studies are evaluating whether CB2 activation further augments VDR signaling and modulates its tumor-suppressive functions in prostate cancer.
利益披露 Disclosure
W. B. Speed, None..
C. V. Hinton, None.