白介素 6 (IL-6) 可以促进前列腺癌 (PCa) 的细胞增殖。全长瞬时受体电位 melastatin 2 (TRPM2-L) 在 PCa 中高度表达。然而，PCa 中 IL-6 和 TRPM2-L 之间的关联尚不清楚。在这里，用10μg/mL托珠单抗（一种IL-6受体（IL-6R）抑制剂）处理人PCa细胞系PC-3和DU-145，细胞中TRPM2-L蛋白表达显着降低。用 TRPM2 短干扰 RNA (siRNA) 稳定转染细胞，细胞存活率明显下降。重组IL-6处理减弱了TRPM2-siRNA对细胞存活的影响。 TRPM2-L 在 PC-3 和 DU-145 细胞中直接与 IL-6R 结合。 PC-3 和 DU-145 细胞中缺氧诱导因子 1α 的蛋白表达可通过 TRPM2-L 的还原而受到抑制。人脐静脉内皮细胞（HUVECs）与PCa细胞间接共培养，与PCa细胞共培养后HUVECs的侵袭和血管生成活性增强。然而，与对照共培养物相比，PCa 细胞中 TRPM2-L 的减少显着降低了 HUVEC 的侵袭和血管生成活性。在体内，使用 PC-3 细胞诱导异种移植肿瘤。托珠单抗治疗或 TRPM2-L 减少明显抑制了肿瘤生长。同时，注射小鼠重组IL-6削弱了TRPM2-L减少的抗肿瘤作用。这些数据表明IL-6/TRPM2-L轴在PCa肿瘤生长中很重要，干扰IL-6/TRPM2-L轴可能是PCa治疗的新方法。

Interleukin-6 (IL-6) can promote cell proliferation in prostate cancer (PCa). Full-length transient receptor potential melastatin 2 (TRPM2-L) is highly expressed in PCa. However, the association between IL-6 and TRPM2-L in PCa is unclear. Here, human PCa cell lines, PC-3 and DU-145, were treated with 10 μg/mL tocilizumab, an IL-6 receptor (IL-6R) inhibitor, and the TRPM2-L protein expression in cells was significantly decreased. Cells were stably transfected with TRPM2 short-interfering RNA (siRNA) and cell survival clearly declined. Recombinant IL-6 treatment weakened the effects of TRPM2-siRNA on cell survival. TRPM2-L binds directly to IL-6R in PC-3 and DU-145 cells. The protein expression of hypoxia-inducible factor-1α was suppressed by reduction with TRPM2-L in PC-3 and DU-145 cells. Human umbilical vein endothelial cells (HUVECs) were indirectly cocultured with PCa cells, and the invasion and angiogenic activity of HUVECs were enhanced after coculture with PCa cells. However, TRPM2-L reduction in PCa cells significantly decreased the invasion and angiogenic activity of HUVECs compared to the control coculture. In vivo, xenograft tumors were induced using PC-3 cells. Tocilizumab treatment or TRPM2-L reduction clearly suppressed tumor growth. Meanwhile, the injection of mouse recombinant IL-6 weakened the antitumor effects of TRPM2-L reduction. These data demonstrate that the IL-6/TRPM2-L axis in PCa tumor growth is important, and interference of the IL-6/TRPM2-L axis may be a novel approach for PCa therapy.