雜志名稱：Nature Communications
影響因子：14.7
文章題目：Ultrasound-triggered and glycosylation inhibition-enhanced tumor piezocatalytic immunotherapy
DOI: https://doi.org/10.1038/s41467-024-53392-1
第一作者：Yinying Pu，Bangguo Zhou，Jinhong Bing，Liang Wang，Mingqi Chen，Yucui Shen，Shuang Gao，Min Zhou，Wencheng Wu，Jianlin Shi
作者單位：
中國(guó)科學(xué)院上海陶瓷研究所
中國(guó)電子科技大學(xué)四川省人民醫(yī)院四川省醫(yī)學(xué)科學(xué)院
浙江大學(xué)醫(yī)學(xué)院附屬第一醫(yī)院
同濟(jì)大學(xué)上海第四人民醫(yī)院
引用YOBIBIO產(chǎn)品：
Phosphate buffer solution (PBS)
Dulbecco’s modified eagle medium (DMEM)
calcein, 4, 6-diamidino-2-phenylindole (DAPI)
propidium iodide (PI)
fluorescein isothiocyanate (FITC)
Superior FBS (U11-020A)
cell counting Kit-8 (CCK-8)
文章摘要：
Nanocatalytic immunotherapy holds excellent potential for future cancer therapy due to its rapid activation of the immune system to attack tumor cells. However, a high level of N-glycosylation can protect tumor cells, compromising the anticancer immunity of nanocatalytic immunotherapy. Here, we show a 2-deoxyglucose (2-DG) and bismuth ferrite co-loaded gel (DBG) scaffold for enhanced cancer piezocatalytic immunotherapy. After the implantation in the tumor, DBG generates both reactive oxygen species (ROS) and piezoelectric signals when excited with ultrasound irradiation, significantly promoting the activation of anticancer immunity. Meanwhile, 2-DG released from ROS-sensitive DBG disrupts the N-glycans synthesis, further overcoming the immunosuppressive microenvironment of tumors. The synergy effects of ultrasound-triggered and glycosylation inhibition enhanced tumor piezocatalytic immunotherapy are demonstrated on four mouse cancer models. A “hot” tumor-immunity niche is produced to inhibit tumor progress and lung metastasis and elicit strong immune memory effects. This work provides a promising piezocatalytic immunotherapy for malignant solid tumors featuring both low immunogenicity and high levels of N-glycosylation.
納米催化免疫療法因其快速激活免疫系統(tǒng)以攻擊腫瘤細(xì)胞而具有極好的未來癌癥治療潛力。然而，高水平的 N-糖基化可以保護(hù)腫瘤細(xì)胞，損害納米催化免疫療法的抗癌免疫力。在這里，我們展示了一種用于增強(qiáng)癌癥壓迫免疫治療的 2-脫氧葡萄糖 （2-DG） 和鐵氧體鉍共負(fù)載凝膠 （DBG） 支架。植入腫瘤后，DBG 在超聲照射下激發(fā)時(shí)產(chǎn)生活性氧 （ROS） 和壓電信號(hào)，顯著促進(jìn)抗癌免疫的激活。同時(shí)，ROS 敏感的 DBG 釋放的 2-DG 破壞了 N-糖的合成，進(jìn)一步克服了腫瘤的免疫抑制微環(huán)境。超聲觸發(fā)和糖基化抑制增強(qiáng)的腫瘤壓電催化免疫療法的協(xié)同作用已在四種小鼠癌癥模型上得到證明。產(chǎn)生“熱”腫瘤免疫生態(tài)位以抑制腫瘤進(jìn)展和肺轉(zhuǎn)移，并引發(fā)強(qiáng)烈的免疫記憶效應(yīng)。這項(xiàng)工作為具有低免疫原性和高水平 N-糖基化的惡性實(shí)體瘤提供了一種有前途的壓電催化免疫療法。
