恶性黑色素瘤是一种起源于黑色素细胞的肿瘤，其特点是在发展的早期阶段动态生长和频繁转移。目前的治疗方法仍然不足，需要寻找治疗这种疾病的新方法。蛋白酶体抑制剂诱导细胞凋亡（生理性细胞死亡）被认为是非侵入性消除癌细胞的有效方法。在我们的研究中，我们想要检查 Marizomib（MZB、salinosporamide A、NPI-0052）（一种源自海洋放线菌热带盐孢菌的不可逆蛋白酶体抑制剂）诱导 A375 和 G361 恶性黑色素瘤细胞凋亡的潜力。我们通过 MTT 测试确定了 Marizomib 的细胞毒活性。溴化乙锭和吖啶橙染色证明了所检查的细胞系中膜完整性的破坏。我们通过流式细胞术并使用 FITC-Annexin V 测定法证实了 marizomib 的促凋亡活性。蛋白质印迹分析显示，与内质网 (ER) 应激相关的蛋白质以及细胞凋亡标记物的表达增加。收集到的研究结果表明，马佐米在所检查的黑色素瘤癌细胞中诱导内质网应激，并将其引导至细胞凋亡途径。

Malignant melanoma-a tumor originating from melanocytes-is characterized by dynamic growth and frequent metastases in the early stage of development. Current therapy methods are still insufficient, and there is a need to search for new ways of treating this malady. The induction of apoptosis-physiological cell death-by proteasome inhibitors is recognized as an effective method of non-invasive elimination of cancer cells. In our research, we wanted to check the potential of marizomib (MZB, salinosporamide A, NPI-0052)-an irreversible proteasome inhibitor derived from the marine actinomycete Salinispora tropica-to induce apoptosis in A375 and G361 malignant melanoma cells. We determined the cytotoxic activity of marizomib by performing an MTT test. Ethidium bromide and acridine orange staining demonstrated the disruption of membrane integrity in the examined cell lines. We confirmed the proapoptotic activity of marizomib by flow cytometry with the use of an FITC-Annexin V assay. A Western blot analysis presented an increase in the expression of proteins related to endoplasmic reticulum (ER) stress as well as markers of the apoptosis. The gathered findings suggest that marizomib induced the ER stress in the examined melanoma cancer cells and directed them towards the apoptosis pathway.