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IgG沉默诱导LNCaP前列腺癌细胞凋亡,并抑制其增殖、迁移和侵袭。

IgG silencing induces apoptosis and suppresses proliferation, migration and invasion in LNCaP prostate cancer cells.

作者信息

Xu Yawen, Chen Binshen, Zheng Shaobo, Wen Yong, Xu Abai, Xu Kai, Li Bingkun, Liu Chunxiao

机构信息

Department of Urology, Zhujiang Hospital, Southern Medical University, No. 253, Industrial Road, Guangzhou, Guangdong China.

出版信息

Cell Mol Biol Lett. 2016 Dec 3;21:27. doi: 10.1186/s11658-016-0029-6. eCollection 2016.

DOI:10.1186/s11658-016-0029-6
PMID:28536629
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5415809/
Abstract

Immunoglobulin G (IgG) has been implicated in the progression of various cancers. This study explored the role of IgG in the proliferation, apoptosis, cell cycle and in vitro invasive properties of LNCaP prostate cancer cells. We used IGHG1 small interfering RNA to silence IgG1 expression in LNCaP cells. The efficacy of IgG1 gene knockdown was confirmed using qPCR and western blotting. The colony formation, proliferation, migration and invasion abilities of LNCaP cells after transfection were assessed using colony-forming, flow cytometry and transwell assays. The expressions of PCNA and caspase-3 proteins in LNCaP cells after transfection were detected with immunofluorescence staining and western blotting. IgG1 silencing significantly decreased the colony formation, survival, cell cycle progression, migration and invasion of LNCaP cells ( < 0.05). IgG1 silencing also reduced the amount of the proliferation marker PCNA and induced formation of the apoptotic marker caspase-3 ( < 0.05). Our results show that IgG1 produced by LNCaP cells confers advantages for tumor cell survival, proliferation, migration and invasion, suggesting that IgG1 is a potential target for prostate cancer treatment.

摘要

免疫球蛋白G(IgG)与多种癌症的进展有关。本研究探讨了IgG在LNCaP前列腺癌细胞增殖、凋亡、细胞周期及体外侵袭特性中的作用。我们使用IGHG1小干扰RNA沉默LNCaP细胞中IgG1的表达。通过qPCR和蛋白质印迹法确认了IgG1基因敲低的效果。使用集落形成、流式细胞术和Transwell实验评估转染后LNCaP细胞的集落形成、增殖、迁移和侵袭能力。通过免疫荧光染色和蛋白质印迹法检测转染后LNCaP细胞中PCNA和caspase-3蛋白的表达。IgG1沉默显著降低了LNCaP细胞的集落形成、存活、细胞周期进程、迁移和侵袭(<0.05)。IgG1沉默还减少了增殖标志物PCNA的量,并诱导了凋亡标志物caspase-3的形成(<0.05)。我们的结果表明,LNCaP细胞产生的IgG1赋予肿瘤细胞存活、增殖、迁移和侵袭优势,提示IgG1是前列腺癌治疗的潜在靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b541/5415809/444cba823ee3/11658_2016_29_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b541/5415809/1a9b65c9c948/11658_2016_29_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b541/5415809/b5f988e924ed/11658_2016_29_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b541/5415809/78f60c244666/11658_2016_29_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b541/5415809/444cba823ee3/11658_2016_29_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b541/5415809/1a9b65c9c948/11658_2016_29_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b541/5415809/b5f988e924ed/11658_2016_29_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b541/5415809/78f60c244666/11658_2016_29_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b541/5415809/444cba823ee3/11658_2016_29_Fig4_HTML.jpg

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