Atezolizumab, a specific monoclonal antibody against PD-L1, can inhibit the combination between PD-L1 and PD-1. Therefore, it showed various promising effects, such as inhibiting the proliferation and induce immune-independent apoptosis of osteosarcoma cells and reducing immunosuppression caused by T lymphocyte apoptosis in various cancer types.[1][2]
In vitro study indicated that atezolizumab could cause mitochondrial damage to induce the imbalance between oxidants and antioxidants and induce mitochondria-related apoptosis in OS cells by activating JNK pathway. Furthermore, atezolizumab induced autophagy, however, inhibition of autophagy enhances atezolizumab-induced apoptosis in osteosarcoma cells.[2]
Study demonstrated that atezolizumab could suppress the proliferation of OS cells in vivo, and the suppression was further enhanced by the combination of CQ. Besides, atezolizumab promoted apoptosis of OS cells in vivo, and this phenomenon was exacerbated by the addition of CQ. Moreover, atezolizumab could increase the content of MDA while increasing the positive rate of ROS in OS.[2]
References:
[1]. Chen J, et al. Atezolizumab alleviates the immunosuppression induced by PD?L1?positive neutrophils and improves the survival of mice during sepsis. Mol Med Rep. 2021 Feb;23(2):144.
[2]. Liu Z, et al. Targeting autophagy enhances atezolizumab-induced mitochondria- related apoptosis in osteosarcoma. Cell Death Dis. 2021 Feb 8;12(2):164.
Atezolizumab 是一种针对 PD-L1 的特异性单克隆抗体,可以抑制 PD-L1 和 PD-1 之间的结合。因此,它显示出多种有前途的作用,例如抑制骨肉瘤细胞的增殖和诱导免疫非依赖性细胞凋亡,以及减轻各种癌症类型中 T 淋巴细胞凋亡引起的免疫抑制。[1][2]\n
体外研究表明,atezolizumab 可引起线粒体损伤,从而导致氧化剂和抗氧化剂之间的失衡,并通过激活 JNK 通路诱导 OS 细胞中线粒体相关的细胞凋亡。此外,atezolizumab 诱导自噬,然而,抑制自噬会增强 atezolizumab 诱导的骨肉瘤细胞凋亡。[2]
研究表明,atezolizumab 可以抑制体内 OS 细胞的增殖,并且通过与 CQ 的组合进一步增强抑制作用。此外,atezolizumab 在体内促进 OS 细胞凋亡,而 CQ 的加入加剧了这种现象。此外,atezolizumab可增加MDA含量,同时提高OS中ROS的阳性率。[2]