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单独的ANTP-SMACN7融合肽在非小细胞肺癌细胞系中诱导了高线性能量转移辐射增敏作用。

ANTP-SMACN7 fusion peptide alone induced high linear energy transfer irradiation radiosensitization in non-small cell lung cancer cell lines.

作者信息

Xie Yi, Wang Bing, Du Liqing, Wang Yan, Xu Chang, Zhang Hong, Wen Kaixue, Liu Qiang, Katsube Takanori

机构信息

Institute of Modern Physics, Chinese Academy of Sciences, Lanzhou 730000, China.

Advanced Energy Science and Technology Guangdong Laboratory, Huizhou 516029, China.

出版信息

Cancer Biol Med. 2021 Sep 21;19(7):983-94. doi: 10.20892/j.issn.2095-3941.2020.0569.

DOI:10.20892/j.issn.2095-3941.2020.0569
PMID:34546667
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9334756/
Abstract

OBJECTIVE

The aim of the present study was to investigate the mechanisms responsible for the radiation-sensitizing effect of antennapedia proteins, ANTP-SMACN7, on lung cancer cells treated with accelerated carbon and Fe particle irradiation.

METHODS

The ANTP-SMACN7 fusion peptide was synthesized and linked to fluorescein isothiocyanate to determine its ability to penetrate cells. A549 and NCI-H460 cells, human non-small cell lung cancer (NSCLC) cell lines, were irradiated with X-ray or high linear energy transfer (LET) irradiation with or without ANTP-SMACN7 treatment. Cellular survival, apoptosis, and protein expression were studied by colony formation assays, flow cytometry, and western blot analyses, respectively.

RESULTS

ANTP-SMACN7 fusion proteins entered the cells and promoted A549 and NCI-H460 cell high LET irradiation radiosensitization. High LET irradiation was more efficient for clonogenic cell killing and the induction of apoptosis ( < 0.05). Treatment with ANTP-SMACN7 significantly reduced the A549 and NCI-H460 cell clone-forming percentages and increased apoptosis through inhibition of the X-linked inhibitor of apoptosis protein and the activation of caspase-3 and caspase-9.

CONCLUSIONS

Regarding pharmaceutical radiosensitization, these findings provided a way to improve high-LET clinical radiotherapy for NSCLC patients.

摘要

目的

本研究旨在探讨触角足蛋白ANTP-SMACN7对接受碳离子和铁粒子加速照射的肺癌细胞产生辐射增敏作用的机制。

方法

合成ANTP-SMACN7融合肽并与异硫氰酸荧光素连接，以确定其穿透细胞的能力。用人非小细胞肺癌（NSCLC）细胞系A549和NCI-H460细胞，在有或无ANTP-SMACN7处理的情况下，进行X射线或高线性能量传递（LET）照射。分别通过集落形成试验、流式细胞术和蛋白质印迹分析研究细胞存活、凋亡和蛋白质表达情况。

结果

ANTP-SMACN7融合蛋白进入细胞并促进A549和NCI-H460细胞的高线性能量传递照射增敏。高线性能量传递照射在克隆细胞杀伤和诱导凋亡方面更有效（<0.05）。ANTP-SMACN7处理显著降低了A549和NCI-H460细胞的克隆形成百分比，并通过抑制凋亡蛋白X连锁抑制剂以及激活半胱天冬酶-3和半胱天冬酶-9增加了细胞凋亡。

结论

关于药物辐射增敏，这些发现为改善NSCLC患者的高线性能量传递临床放射治疗提供了一种方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98ca/9334756/e63b346cd020/cbm-19-983-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98ca/9334756/145cface3f7b/cbm-19-983-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98ca/9334756/bbae6bbe2e6c/cbm-19-983-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98ca/9334756/5d36a93bb596/cbm-19-983-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98ca/9334756/e63b346cd020/cbm-19-983-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98ca/9334756/145cface3f7b/cbm-19-983-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98ca/9334756/bbae6bbe2e6c/cbm-19-983-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98ca/9334756/5d36a93bb596/cbm-19-983-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98ca/9334756/e63b346cd020/cbm-19-983-g004.jpg

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