Department of Medicine, Tulane University School of Medicine, New Orleans, LA 70112, USA.
Weill Cornell Medicine-Qatar, Education City, Qatar Foundation, P.O. Box 24144, Qatar.
Life Sci. 2024 Dec 1;358:123125. doi: 10.1016/j.lfs.2024.123125. Epub 2024 Oct 15.
The ubiquitin-proteasome pathway (UPP) regulates protein stability and normal cellular functions with the help of autocatalytic proteasome complex. Studies have linked aberrant proteasome activity to malignant cells and found that proteasome inhibitors play a significant role as therapeutic drugs for various types of cancer, specifically multiple myeloma and mantle cell lymphoma. Bortezomib, the first FDA-approved proteasome inhibitor for treating different stages of multiple myeloma, acts on cancer cells by inhibiting the 26S proteasome, modulating NF-κB, phosphorylating Bcl-2, upregulating of NOXA, blocking p53 degradation, activating caspase, generating reactive oxygen species (ROS), and inhibiting angiogenesis. However, its efficacy is limited due to side effects such as peripheral neuropathy (PN), thrombotic microangiopathy (TMA), and acute interstitial nephritis (AIN). Therefore, a better understanding of its precise mechanism of action may help mitigate these side effects. In this review, we have discussed the proposed mechanisms of action and off target effects of Bortezomib, along with the prospects of next generation potential proteasome inhibitor drugs in the treatment of cancer.
泛素-蛋白酶体途径 (UPP) 在自体催化蛋白酶体复合物的帮助下调节蛋白质稳定性和正常细胞功能。研究表明,异常的蛋白酶体活性与恶性细胞有关,并发现蛋白酶体抑制剂作为治疗各种类型癌症(特别是多发性骨髓瘤和套细胞淋巴瘤)的药物具有重要作用。硼替佐米是第一个获得 FDA 批准用于治疗多发性骨髓瘤不同阶段的蛋白酶体抑制剂,通过抑制 26S 蛋白酶体、调节 NF-κB、磷酸化 Bcl-2、上调 NOXA、阻断 p53 降解、激活半胱天冬酶、产生活性氧 (ROS) 和抑制血管生成来作用于癌细胞。然而,由于周围神经病变 (PN)、血栓性微血管病 (TMA) 和急性间质性肾炎 (AIN) 等副作用,其疗效受到限制。因此,更好地了解其确切的作用机制可能有助于减轻这些副作用。在这篇综述中,我们讨论了硼替佐米的作用机制和脱靶效应的推测机制,以及下一代潜在蛋白酶体抑制剂药物在癌症治疗中的前景。