中文摘要
本研究旨在通过Panc02细胞荷瘤小鼠模型在体内探讨细胞因子诱导的杀伤(CIK)细胞联合不可逆电穿孔(IRE)的抗肿瘤作用及其有效机制。从Panc02胰腺癌(PC)皮下异种移植模型小鼠的脾脏中分离CIK细胞,并测定不同淋巴细胞的比例。同时研究IRE联合CIK细胞在PC皮下异种移植模型中的抗肿瘤效果。体外培养21天后,CD3+CD8+阳性细胞比例和CD3+CD56+细胞比例均显著增加。IRE联合CIK细胞治疗显著抑制了肿瘤生长,并提高了Panc02细胞荷瘤小鼠的生存率。此外,与未治疗组或单药治疗组相比,该联合治疗显著增加了淋巴细胞向肿瘤组织的浸润。另外,IRE显著增强了CIK细胞所引发的趋化因子受体的表达。总之,IRE联合CIK细胞在PC异种移植模型中显示出优越的抗肿瘤疗效,我们将其归因于促进淋巴细胞浸润,以及上调趋化因子受体表达和CIK细胞增殖的调节因子。
展开英文摘要原文
The current study aimed to investigate the antitumor effects and potent mechanism of cytokine-induced killer (CIK) cells combined with irreversible electroporation (IRE) via Panc02 cell-bearing mouse model in vivo. CIK cells were isolated from the spleens of Panc02 pancreatic-cancer (PC) subcutaneous-xenograft model and the proportion of different lymphocytes was also determined.
The antitumor effect of the combination of IRE and CIK cells in a PC subcutaneous-xenograft model was also investigated. The proportion of cells that were positive for CD3 + CD8 + and the proportion of CD3 + CD56 + cells were both significantly increased after 21 days of in vitro culture. Combined treatment of IRE and CIK cell significantly inhibited tumor growth and increased the survival rate of Panc02 cell-bearing mice.
Furthermore, infiltration of lymphocytes into tumor tissue was significantly increased by this combination therapy compared with the untreated group or monotherapy group.
In addition, IRE significantly enhanced the expression of chemokine receptors elicited by CIK cells.
In conclusion, IRE combined with CIK cells showed superior antitumor efficacy in a PC xenograft model, which we attributed to the promotion of lymphocytic infiltration, as well as to upregulation of chemokine receptor expression and the regulators of CIK cell proliferation.
论文信息
- 作者
- Wang B、Wang H、Yue L、Chen Q、Dong J、Jiang T
- 单位
- Department of Ultrasound Medicine, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310003, China.China
- 期刊
- Biochemistry and biophysics reports2023 Sep