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首页> 外文期刊>Journal of dermatological science >N-propionyl-4-S-cysteaminylphenol induces apoptosis in B16F1 cells and mediates tumor-specific T-cell immune responses in a mouse melanoma model
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N-propionyl-4-S-cysteaminylphenol induces apoptosis in B16F1 cells and mediates tumor-specific T-cell immune responses in a mouse melanoma model

机译：N-丙酰-4-S-半胱氨酰苯酚在小鼠黑素瘤模型中诱导B16F1细胞凋亡并介导肿瘤特异性T细胞免疫应答

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Background: N-propionyl-4- S-cysteaminylphenol (NPr-4- S-CAP) is selectively incorporated into melanoma cells and degrades them. However, it remains unclear whether NPr-4- S-CAP can induce cell death associated with the induction of host immune responses and tumor suppression in vivo. Objective: To examine the molecular mechanism of NPr-4- S-CAP-mediated cytotoxicity toward melanoma cells and to test whether NPr-4- S-CAP can suppress transplanted primary and secondary B16F1 melanomas. Methods: Cytotoxicity and apoptosis of melanoma cells were assessed by cell counting, flow cytometry, and detection of reactive oxygen species (ROS) and apoptotic molecules. NPr-4- S-CAP-associated host immunity was studied using a B16F1 mouse melanoma model through the application of CD4- and CD8-specific antibodies and tetramer assay. Results: NPr-4-S-CAP suppressed growth of pigmented melanoma cells associated with an increase of intracellular ROS, activation of caspase 3 and DNA fragmentation, suggesting that NPr-4-S-CAP mediated ROS production, eliciting apoptosis of melanoma cells. Growth of transplanted B16F1 melanomas was inhibited after the consecutive intratumoral injections of NPr-4-S-CAP, and the tumor growth after rechallenge of B16F1 was significantly suppressed in the treated mice. This suppression occurred when the treated mice were given the anti-CD4 antibody, but not the anti-CD8 antibody. Tetramer assay demonstrated increased TYRP-2-specific CD8 + T cells in the lymph node and spleen cells prepared from NPr-4-S-CAP-treated B16F1-bearing mice. Conclusions: These suggest that NPr-4-S-CAP induces apoptosis in melanoma cells through ROS production and generates CD8 + cell immunity resulting in the suppression of rechallenged B16F1 melanoma.
机译：背景：N-丙酰基-4-S-半胱氨酰苯酚（NPr-4-S-CAP）被选择性地掺入黑色素瘤细胞并使之降解。然而，目前尚不清楚NPr-4-S-CAP是否可以在体内诱导宿主免疫应答和抑制肿瘤相关的细胞死亡。目的：探讨NPr-4-S-CAP介导的黑色素瘤细胞毒性的分子机制，并探讨NPr-4-S-CAP能否抑制原发性和继发性B16F1黑素瘤的移植。方法：通过细胞计数，流式细胞术以及检测活性氧（ROS）和凋亡分子的方法评估黑素瘤细胞的细胞毒性和凋亡。使用B16F1小鼠黑素瘤模型，通过应用CD4和CD8特异性抗体并进行四聚体分析，研究了与NPr-4- S-CAP相关的宿主免疫。结果：NPr-4-S-CAP抑制了色素沉着的黑素瘤细胞的生长，与细胞内ROS的增加，胱天蛋白酶3的活化和DNA片段化有关，这表明NPr-4-S-CAP介导了ROS的产生，引发了黑素瘤细胞的凋亡。连续瘤内注射NPr-4-S-CAP后，移植的B16F1黑色素瘤的生长受到抑制，在接受治疗的小鼠中，B16F1再挑战后的肿瘤生长得到显着抑制。当给予治疗的小鼠抗CD4抗体而非抗CD8抗体时，就会出现这种抑制作用。四聚体分析表明，从用NPr-4-S-CAP处理的B16F1小鼠制备的淋巴结和脾细胞中，TYRP-2特异性CD8 + T细胞增加。结论：这些提示NPr-4-S-CAP通过产生ROS诱导黑素瘤细胞凋亡，并产生CD8 +细胞免疫力，从而抑制了再挑战的B16F1黑素瘤。

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