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在非小细胞肺癌大鼠模型中，抑制miR-22增强了埃克替尼联合培美曲塞的疗效。

Inhibition of miR-22 enhanced the efficacy of icotinib plus pemetrexed in a rat model of non-small cell lung cancer.

作者信息

Zhang Jing, Xue Zhi-Qiang, Wang Bin, Wen Jia-Xin, Wang Yun-Xi

机构信息

Department of Thoracic Surgery, The First Medical Center of Chinese PLA General Hospital, Beijing 100853, China.

出版信息

Iran J Basic Med Sci. 2020 Mar;23(3):329-336. doi: 10.22038/IJBMS.2019.39291.9320.

DOI:10.22038/IJBMS.2019.39291.9320
PMID:32440319
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7229502/
Abstract

OBJECTIVES

To investigate the role of miR-22 in the efficacy of combined icotinib (BPI-2009H) and pemetrexed (LY-231514) on tumor growth and apoptosis in rats with non-small cell lung cancer (NSCLC).

MATERIALS AND METHODS

Rats were injected with HCC827 cells, which were transfected with anti-miR-22, followed by the treatment of BPI-2009H and/or LY-231514. MTT assay was used to detect the inhibition rate of HCC827 cells. qRT-PCR was performed to examine miR-22 expression in HCC827 cells and lung tumor tissues. Moreover, immunohistochemistry and Western blotting were performed to detect the related-molecule expressions, while TUNEL staining was used to observe cell apoptosis of lung tumor tissues.

RESULTS

MiR-22 expression was decreased in HCC827 cells after the treatment of BPI-2009H or LY-231514 in a dose-dependent manner. Both BPI-2009H and LY-231514 increased the inhibition rate of HCC827 cells, which was enhanced by anti-miR-22 with decreased IC50 values. Furthermore, the decreased expression of miR-22 was found after the treatment of BPI-2009H or/and LY-231514 in lung tumor tissues. In addition, the expressions of PCNA, Ki67, and Bcl-2 were reduced, but Bax and Caspase-3 were increased in treated rats, typically in those rats treated with the combination of anti-miR-22, BPI-2009H, and LY-231514.

CONCLUSION

Inhibition of miR-22 could enhance the efficacy of icotinib combined with pemetrexed in rats with NSCLC, providing a new perspective for NSCLC therapy.

摘要

目的

探讨miR-22在埃克替尼（BPI-2009H）联合培美曲塞（LY-231514）对非小细胞肺癌（NSCLC）大鼠肿瘤生长及凋亡影响中的作用。

材料与方法

将转染了抗miR-22的HCC827细胞注射到大鼠体内，随后给予BPI-2009H和/或LY-231514治疗。采用MTT法检测HCC827细胞的抑制率。运用qRT-PCR检测HCC827细胞及肺肿瘤组织中miR-22的表达。此外，采用免疫组化和蛋白质印迹法检测相关分子的表达，同时运用TUNEL染色观察肺肿瘤组织的细胞凋亡情况。

结果

BPI-2009H或LY-231514处理后，HCC827细胞中miR-22的表达呈剂量依赖性降低。BPI-2009H和LY-231514均提高了HCC827细胞的抑制率，抗miR-22使其增强，IC50值降低。此外，BPI-2009H或/和LY-231514处理后，肺肿瘤组织中miR-22表达降低。另外，处理后的大鼠中PCNA、Ki67和Bcl-2的表达降低，但Bax和Caspase-3的表达增加，尤其是在联合抗miR-22、BPI-2009H和LY-231514处理的大鼠中。

结论

抑制miR-22可增强埃克替尼联合培美曲塞对NSCLC大鼠的疗效，为NSCLC治疗提供了新的视角。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f12/7229502/b115c8ef0688/IJBMS-23-329-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f12/7229502/5bd0cc34f20e/IJBMS-23-329-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f12/7229502/97225147bf82/IJBMS-23-329-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f12/7229502/5ab7a63dde26/IJBMS-23-329-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f12/7229502/af4fffb37019/IJBMS-23-329-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f12/7229502/1107f0a63e19/IJBMS-23-329-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f12/7229502/b115c8ef0688/IJBMS-23-329-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f12/7229502/5bd0cc34f20e/IJBMS-23-329-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f12/7229502/97225147bf82/IJBMS-23-329-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f12/7229502/5ab7a63dde26/IJBMS-23-329-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f12/7229502/af4fffb37019/IJBMS-23-329-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f12/7229502/1107f0a63e19/IJBMS-23-329-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f12/7229502/b115c8ef0688/IJBMS-23-329-g006.jpg

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