通过调控MAGEC2对非小细胞肺癌血管生成及上皮-间质转化的抑制作用研究
Study on Attenuating Angiogenesis and Epithelial-Mesenchymal Transition (EMT) of Non-Small Cell Lung Carcinoma (NSCLC) by Regulating MAGEC2.
作者信息
Jiang Sicong, Liu Xi, Li Daojing, Yan Meiying, Ju Cheng, Sun Jun, Jiang Feng
机构信息
1 Department of Thoracic Surgery, Medical College of Nanchang University, Nanchang, Jiangxi, China.
2 Department of Thoracic Surgery, Jiangxi Province Tumor Hospital, Nanchang, Jiangxi, China.
出版信息
Technol Cancer Res Treat. 2018 Jan 1;17:1533033818797587. doi: 10.1177/1533033818797587.
OBJECTIVE
To investigate the role of MAGE family member C2 in angiogenesis and epithelial-mesenchymal transition of non-small cell lung carcinoma.
METHODS
The Cancer Genome Atlas data set was analyzed to filter the highly expressed gene melanoma antigen family C2 in non-small cell lung carcinoma. Quantitative reverse transcription-polymerase chain reaction was performed to verify the overexpression of melanoma antigen family C2 in non-small cell lung carcinoma cell lines. Melanoma antigen family C2 complementary DNA and short hairpin RNA (shRNA) were transfected into SK-MES-1 cells to regulate melanoma antigen family C2 expression. Cell Counting Kit-8 assay, flow cytometry, wound healing assay, and Transwell assay were performed to investigate the effect of melanoma antigen family C2 on proliferation, apoptosis, migration, and invasion of SK-MES-1 cell line. Western blot was used to detect the expression of epithelial-mesenchymal transition markers. Enzyme-linked immunosorbent assay was performed to investigate the secretion of vascular endothelial growth factor, and tube formation assay was conducted to explore the effect of melanoma antigen family C2 on angiogenesis ability of the tumor. Tumor xenograft on nude mice and immunohistochemical/hematoxylin and eosin staining were also performed to detect the influence of melanoma antigen family C2 on growth and metastasis of non-small cell lung carcinoma cells.
RESULTS
Melanoma antigen family C2 was highly expressed in non-small cell lung carcinoma cells; melanoma antigen family C2 promoted the expression of epithelial-mesenchymal transition-related proteins as well as enhance the secretion of vascular endothelial growth factor and promote angiogenesis; melanoma antigen family C2 promoted proliferation, migration, and invasion and suppressed apoptosis of non-small cell lung carcinoma cells. It could also facilitate growth and metastasis of non-small cell lung carcinoma in vivo.
CONCLUSION
Melanoma antigen family C2 was a critical factor of angiogenesis and epithelial-mesenchymal transition in non-small cell lung carcinoma.
目的
探讨黑色素瘤抗原家族成员C2（MAGE - C2）在非小细胞肺癌血管生成和上皮-间质转化中的作用。
方法
分析癌症基因组图谱数据集，筛选出在非小细胞肺癌中高表达的基因MAGE - C2。采用定量逆转录-聚合酶链反应验证MAGE - C2在非小细胞肺癌细胞系中的过表达情况。将MAGE - C2互补DNA及短发夹RNA（shRNA）转染至SK - MES - 1细胞，以调节MAGE - C2表达。运用细胞计数试剂盒-8法、流式细胞术、伤口愈合实验及Transwell实验，研究MAGE - C2对SK - MES - 1细胞系增殖、凋亡、迁移及侵袭的影响。采用蛋白质免疫印迹法检测上皮-间质转化标志物的表达。通过酶联免疫吸附测定法研究血管内皮生长因子的分泌情况，并进行管腔形成实验，以探究MAGE - C2对肿瘤血管生成能力的影响。还进行了裸鼠肿瘤异种移植及免疫组织化学/苏木精-伊红染色，以检测MAGE - C2对非小细胞肺癌细胞生长和转移的影响。
结果
MAGE - C2在非小细胞肺癌细胞中高表达；MAGE - C2促进上皮-间质转化相关蛋白的表达，增强血管内皮生长因子的分泌并促进血管生成；MAGE - C2促进非小细胞肺癌细胞的增殖、迁移和侵袭，抑制其凋亡。在体内它还可促进非小细胞肺癌的生长和转移。
结论
MAGE - C2是非小细胞肺癌血管生成和上皮-间质转化的关键因子。
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