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在Plk1和HDAC联合抑制后，原代细胞存活，但癌细胞不存活。

Survival of primary, but not of cancer cells after combined Plk1-HDAC inhibition.

作者信息

Lange Lisa, Hemmerich Peter, Spänkuch Birgit

机构信息

Friedrich-Schiller-University, CMB, Institute for Biochemistry and Biophysics, 07745 Jena, Germany.

Leibniz-Institute for Age Research-Fritz Lipmann Institute, JenAge (Jena Centre for Systems Biology of Aging), 07745 Jena, Germany.

出版信息

Oncotarget. 2015 Sep 22;6(28):25801-14. doi: 10.18632/oncotarget.4445.

DOI:10.18632/oncotarget.4445
PMID:26317649
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4694867/
Abstract

In the current study we examined the combination of SAHA and SBE13 in cancer and non-cancer cells. HeLa cells displayed a synergistically reduced cell proliferation, which was much weaker in hTERT-RPE1 or NIH-3T3 cells. Cell cycle distribution differed in HeLa, hTERT-RPE1 and NIH-3T3 cells. SAHA-treated HeLa cells showed slightly increasing cell numbers in G2/M phase, but after combination with SBE13 strongly elevated cell numbers in G2/M and S phase, accompanied by decreasing G0/G1 percentages. hTERT-RPE1 and NIH-3T3 cells showed strongly enriched cell numbers in G0/G1 phase. Western blot and quantitative real time analyses revealed reduced Plk1 mRNA and protein in all cells. p21 protein was strongly induced in cancer, but not in non-cancer cells, corresponding to a different localization in immunofluorescence studies. Additionally, these revealed an abundantly present pRb protein in HeLa cells after any treatment but almost completely vanished pRb staining in treated hTERT-RPE1 cells. These differences could be approved in Western blots against Parp and Caspase 3, which were activated in HeLa, but not in hTERT-RPE1 cells. Thus, we observed for the first time a differential effect of cancer versus non-cancer cells after treatment with SAHA and SBE13, which might be due to the dual role of p21.

摘要

在本研究中，我们检测了SAHA和SBE13联合作用于癌细胞和非癌细胞的情况。HeLa细胞的增殖呈现协同性降低，而在hTERT-RPE1或NIH-3T3细胞中这种作用则弱得多。HeLa、hTERT-RPE1和NIH-3T3细胞的细胞周期分布有所不同。经SAHA处理的HeLa细胞在G2/M期的细胞数量略有增加，但与SBE13联合处理后，G2/M期和S期的细胞数量大幅增加，同时G0/G1期的百分比下降。hTERT-RPE1和NIH-3T3细胞在G0/G1期的细胞数量显著增加。蛋白质免疫印迹和定量实时分析显示，所有细胞中Plk1的mRNA和蛋白水平均降低。p21蛋白在癌细胞中被强烈诱导，但在非癌细胞中未被诱导，这与免疫荧光研究中的不同定位一致。此外，这些研究还显示，任何处理后HeLa细胞中均大量存在pRb蛋白，但在处理后的hTERT-RPE1细胞中pRb染色几乎完全消失。这些差异在针对Parp和Caspase 3的蛋白质免疫印迹中得到证实，它们在HeLa细胞中被激活，但在hTERT-RPE1细胞中未被激活。因此，我们首次观察到SAHA和SBE13处理后癌细胞与非癌细胞存在差异效应，这可能归因于p21的双重作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aca8/4694867/8cf613b1d381/oncotarget-06-25801-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aca8/4694867/890701dc5473/oncotarget-06-25801-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aca8/4694867/90cfceecd646/oncotarget-06-25801-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aca8/4694867/e3439fc5e3f3/oncotarget-06-25801-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aca8/4694867/7304327555c5/oncotarget-06-25801-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aca8/4694867/fdd62212b508/oncotarget-06-25801-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aca8/4694867/8cf613b1d381/oncotarget-06-25801-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aca8/4694867/890701dc5473/oncotarget-06-25801-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aca8/4694867/90cfceecd646/oncotarget-06-25801-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aca8/4694867/e3439fc5e3f3/oncotarget-06-25801-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aca8/4694867/7304327555c5/oncotarget-06-25801-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aca8/4694867/fdd62212b508/oncotarget-06-25801-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aca8/4694867/8cf613b1d381/oncotarget-06-25801-g006.jpg

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Oncogene. 2015 Apr 2;34(14):1758-67. doi: 10.1038/onc.2014.133. Epub 2014 May 26.
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