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褪黑素通过激活ERK1/2信号通路诱导金属硫蛋白-2表达，从而促进GC-1 spg细胞的增殖。

Melatonin promotes the proliferation of GC-1 spg cells by inducing metallothionein-2 expression through ERK1/2 signaling pathway activation.

作者信息

Li Chunjin, Zhu Xiaoling, Chen Shuxiong, Chen Lu, Zhao Yun, Jiang Yanwen, Gao Shan, Wang Fengge, Liu Zhuo, Fan Rong, Sun Liting, Zhou Xu

机构信息

College of Animal Sciences, Jilin Provincial Key Laboratory of Animal Embryo Engineering, Jilin University, Changchun, Jilin, 130062, P.R. China.

出版信息

Oncotarget. 2017 Aug 7;8(39):65627-65641. doi: 10.18632/oncotarget.20019. eCollection 2017 Sep 12.

DOI:10.18632/oncotarget.20019
PMID:29029459
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5630359/
Abstract

Synthesized by the pineal gland, melatonin is a neurohormone implicated in diverse physiological functions via several mechanisms. However, the role of melatonin in spermatogenesis and its underlying mechanisms have yet to be completely understood. In the present study, transcriptome sequencing was performed to characterize the mechanism of melatonin-induced GC-1 spg proliferation. Gene ontology (GO) enrichment and pathway analyses were also conducted to identify the signaling pathways and biological processes involved in differential mRNA expression. Results revealed 28 differential genes. Of these genes, 11 were upregulated and 17 were downregulated. Melatonin increased the expression of metallothionein-2 (), a gene that acts as a protector to sequester nonessential toxic heavy metals. Functional investigations demonstrated that overexpression promoted the proliferation of GC-1 spg cells, but knockdown significantly suppressed their proliferation and increased their apoptosis. Mechanistic analysis indicated that the extracellular-signal-regulated kinase 1/2 (ERK1/2) pathway participated in melatonin-promoted proliferation of GC-1 spg cells. Therefore, melatonin induces the proliferation of GC-spg 1 cells by stimulating expression, and this process is mediated by the ERK1/2 signaling pathway.

摘要

褪黑素由松果体合成，是一种通过多种机制参与多种生理功能的神经激素。然而，褪黑素在精子发生中的作用及其潜在机制尚未完全明确。在本研究中，进行了转录组测序以表征褪黑素诱导GC-1 spg细胞增殖的机制。还进行了基因本体（GO）富集和通路分析，以鉴定差异mRNA表达所涉及的信号通路和生物学过程。结果显示有28个差异基因。其中，11个基因上调，17个基因下调。褪黑素增加了金属硫蛋白-2（）的表达，该基因作为一种保护因子可螯合非必需的有毒重金属。功能研究表明，金属硫蛋白-2过表达促进了GC-1 spg细胞的增殖，但敲低则显著抑制其增殖并增加其凋亡。机制分析表明，细胞外信号调节激酶1/2（ERK1/2）通路参与了褪黑素促进的GC-1 spg细胞增殖。因此，褪黑素通过刺激金属硫蛋白-2表达诱导GC-1 spg细胞增殖，并且这一过程由ERK1/2信号通路介导。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa3b/5630359/b8adc81e6d03/oncotarget-08-65627-g011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa3b/5630359/ea3cad4461f0/oncotarget-08-65627-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa3b/5630359/df212bc649ea/oncotarget-08-65627-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa3b/5630359/b9025e7aec9c/oncotarget-08-65627-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa3b/5630359/903ac074b5a4/oncotarget-08-65627-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa3b/5630359/518242a4e3b2/oncotarget-08-65627-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa3b/5630359/b4e04c604b17/oncotarget-08-65627-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa3b/5630359/cb06e9720ba8/oncotarget-08-65627-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa3b/5630359/c7b712f6afb9/oncotarget-08-65627-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa3b/5630359/4f2f65533806/oncotarget-08-65627-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa3b/5630359/3cb96f683913/oncotarget-08-65627-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa3b/5630359/b8adc81e6d03/oncotarget-08-65627-g011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa3b/5630359/ea3cad4461f0/oncotarget-08-65627-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa3b/5630359/df212bc649ea/oncotarget-08-65627-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa3b/5630359/b9025e7aec9c/oncotarget-08-65627-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa3b/5630359/903ac074b5a4/oncotarget-08-65627-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa3b/5630359/518242a4e3b2/oncotarget-08-65627-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa3b/5630359/b4e04c604b17/oncotarget-08-65627-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa3b/5630359/cb06e9720ba8/oncotarget-08-65627-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa3b/5630359/c7b712f6afb9/oncotarget-08-65627-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa3b/5630359/4f2f65533806/oncotarget-08-65627-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa3b/5630359/3cb96f683913/oncotarget-08-65627-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa3b/5630359/b8adc81e6d03/oncotarget-08-65627-g011.jpg

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