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携带TRAIL-IETD-MnSOD的溶瘤腺病毒ZD55与细胞因子诱导的杀伤细胞联合治疗肺癌。

Combination of oncolytic adenovirus ZD55 harboring TRAIL-IETD-MnSOD and cytokine-induced killer cells against lung cancer.

作者信息

Jiang Runde, Zhang Zhixiong, Liao Xinghai, Huang Liangjuan, Liao Yilang, Deng Weiyi

机构信息

Department of Pathology, Shenzhen Hospital of Southern Medical University, Shenzhen, China.

出版信息

Ann Transl Med. 2021 Oct;9(20):1527. doi: 10.21037/atm-21-4479.

DOI:10.21037/atm-21-4479
PMID:34790733
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8576688/
Abstract

BACKGROUND

Our study aimed to investigate the effect of cancer-targeting gene-virotherapy and cytokine-induced killer (CIK) cell immunotherapy on lung cancer.

METHODS

CIK cells were obtained from peripheral blood mononuclear cells using interferon (IFN)-γ, interleukin (IL)-2, and CD3 monoclonal antibody. The CIK cells were infected with oncolytic adenovirus ZD55 harboring tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL), manganese-containing superoxide dismutase (MnSOD), and TRAIL-isoleucine-aspartate-threonine-glutamate (IETD)-MnSOD. The cells were then cocultured with lung cancer cell lines A549 and NCI-H1650, normal cell line BEAS-2B, or injected into an A549 xenograft mouse model.

RESULTS

Proliferation, colony formation, and invasion of A549 and NCI-H1650 cells were significantly inhibited by co-cultivation with CIK cells carrying oncolytic adenoviruses (in order) ZD55-TRAIL-IETD-MnSOD > ZD55-TRAIL + ZD55-MnSOD > ZD55-MnSOD > ZD55-TRAIL. Compared to BEAS-2B cells, the production of IFN-γ, TNF-α, and lactate dehydrogenase (LDH) in tumor cells was increased. Tumor volume in the xenograft model and Ki-67 expression in tumor samples were reduced after injection of CIK cells carrying oncolytic adenoviruses, in the same order as the experiments. Levels of IFN-γ, TNF-α, and LDH contents were also increased in the same order.

CONCLUSIONS

Our studies confirmed the high efficacy of combined oncolytic adenovirus ZD55 harboring TRAIL-IETD-MnSOD and CIK cells against lung cancer.

摘要

背景

我们的研究旨在探讨靶向癌症的基因病毒疗法和细胞因子诱导的杀伤（CIK）细胞免疫疗法对肺癌的影响。

方法

使用干扰素（IFN）-γ、白细胞介素（IL）-2和CD3单克隆抗体从外周血单个核细胞中获取CIK细胞。用携带肿瘤坏死因子（TNF）相关凋亡诱导配体（TRAIL）、含锰超氧化物歧化酶（MnSOD）以及TRAIL-异亮氨酸-天冬氨酸-苏氨酸-谷氨酸（IETD）-MnSOD的溶瘤腺病毒ZD55感染CIK细胞。然后将这些细胞与肺癌细胞系A549和NCI-H1650、正常细胞系BEAS-2B共培养，或注射到A549异种移植小鼠模型中。

结果

与携带溶瘤腺病毒（依次为）ZD55-TRAIL-IETD-MnSOD > ZD55-TRAIL + ZD55-MnSOD > ZD55-MnSOD > ZD55-TRAIL的CIK细胞共培养后，A549和NCI-H1650细胞的增殖、集落形成和侵袭受到显著抑制。与BEAS-2B细胞相比，肿瘤细胞中IFN-γ、TNF-α和乳酸脱氢酶（LDH）的产生增加。注射携带溶瘤腺病毒的CIK细胞后，异种移植模型中的肿瘤体积和肿瘤样本中的Ki-67表达降低，顺序与实验相同。IFN-γ、TNF-α水平和LDH含量也按相同顺序增加。

结论

我们的研究证实了携带TRAIL-IETD-MnSOD的溶瘤腺病毒ZD55与CIK细胞联合使用对肺癌具有高效性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7610/8576688/c812fc5b5f16/atm-09-20-1527-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7610/8576688/c7085fe5d41f/atm-09-20-1527-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7610/8576688/2eec729b4f4c/atm-09-20-1527-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7610/8576688/a2fb3539b9fa/atm-09-20-1527-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7610/8576688/529ceeb00644/atm-09-20-1527-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7610/8576688/c812fc5b5f16/atm-09-20-1527-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7610/8576688/c7085fe5d41f/atm-09-20-1527-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7610/8576688/2eec729b4f4c/atm-09-20-1527-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7610/8576688/a2fb3539b9fa/atm-09-20-1527-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7610/8576688/529ceeb00644/atm-09-20-1527-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7610/8576688/c812fc5b5f16/atm-09-20-1527-f5.jpg

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