口服脊髓灰质炎病毒疫苗诱导的程序性细胞死亡涉及人类结直肠癌癌症细胞的内在和外在途径。

IF 6.7
Oncolytic Virotherapy Pub Date : 2018-10-30 eCollection Date: 2018-01-01 DOI:10.2147/OV.S177260
Sareh Zhand, Seyed Masoud Hosseini, Alijan Tabarraei, Mohsen Saeidi, Marie Saghaeian Jazi, Mohamad Reza Kalani, Abdolvahab Moradi
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引用次数: 0

摘要

目的:癌症(CRC)是全球癌症死亡最常见的原因之一。复制能力强的病毒,自然能够感染和裂解肿瘤细胞,似乎在这个领域很有前景。本研究的目的是评估口服脊髓灰质炎病毒疫苗(OPV)对人结直肠癌细胞的潜力,并阐明其诱导凋亡的机制。材料和方法:分别用流式细胞仪和SYBR Green实时聚合酶链式反应检测脊髓灰质炎病毒(PV)受体(CD155)在HCT116、SW480、HT-29和Caco-2四种人CRC细胞系和正常胎儿人结肠(FHC)细胞系上的蛋白和基因表达。用MTT法检测OPV对指示细胞系的细胞毒性。使用胱天蛋白酶-8和胱天蛋白酶-9比色测定试剂盒检测OPV对内源性和外源性途径的细胞凋亡诱导能力。研究了PV在上述细胞系中的增殖,并用TaqMan PCR测定了病毒产量(细胞相关和细胞外)。结果:CD155mRNA和蛋白在所研究的CRC细胞系中表达显著高于正常细胞系(P=0.0)。OPV在人CRC细胞中以时间和剂量依赖的方式诱导细胞死亡。在CRC细胞中检测到通过外在和内在途径的细胞凋亡,在FHC中发现最低水平。PV病毒载量通过外源性(R=0.945,P=0.0001)和内源性(R=0.756,P=0.001)途径与细胞凋亡显著相关。结论:OPV在CRC的临床治疗中具有一定的应用潜力。然而,需要在动物模型(肿瘤异种移植物)中进行进一步的研究,以确定其是否足以用于CRC的治疗。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Oral poliovirus vaccine-induced programmed cell death involves both intrinsic and extrinsic pathways in human colorectal cancer cells.

Oral poliovirus vaccine-induced programmed cell death involves both intrinsic and extrinsic pathways in human colorectal cancer cells.

Oral poliovirus vaccine-induced programmed cell death involves both intrinsic and extrinsic pathways in human colorectal cancer cells.

Oral poliovirus vaccine-induced programmed cell death involves both intrinsic and extrinsic pathways in human colorectal cancer cells.

Purpose: Colorectal cancer (CRC) is one of the most common causes of cancer death throughout the world. Replication-competent viruses, which are naturally able to infect and lyse tumor cells, seem to be promising in this field. The aim of this study was to evaluate the potential of oral poliovirus vaccine (OPV) on human CRC cells and elucidate the mechanism of apoptosis induction.

Materials and methods: Protein and gene expression of poliovirus (PV) receptor (CD155) on four human CRC cell lines including HCT116, SW480, HT-29, and Caco-2 and normal fetal human colon (FHC) cell line as a control were examined by flow cytometry and SYBR Green Real-Time PCR, respectively. Cytotoxicity of OPV on indicated cell lines was tested using MTT assay. The ability of OPV on apoptosis induction for both intrinsic and extrinsic pathways was examined using caspase-8 and caspase-9 colorimetric assay kits. The PV propagation in mentioned cell lines was investigated, and the quantity of viral yields (cells associated and extracellular) was determined using TaqMan PCR.

Results: CD155 mRNA and protein were expressed significantly higher in studied CRC cell lines rather than the normal cell line (P=0). OPV induced cell death in a time- and dose-dependent manner in human CRC cells. Apoptosis through both extrinsic and intrinsic pathways was detected in CRC cells with the minimum level found in FHC. PV viral load was significantly correlated with apoptosis via extrinsic (R=0.945, P=0.0001) and intrinsic (R=0.756, P=0.001) pathways.

Conclusion: This study suggests that OPV has potential for clinical treatment of CRC. However further studies in animal models (tumor xenografts) are needed to be certain that it is qualified enough for treatment of CRC.

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