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非小细胞肺癌细胞对lunasin的敏感性与整合素信号传导的抑制以及组蛋白乙酰化的变化有关。

Lunasin sensitivity in non-small cell lung cancer cells is linked to suppression of integrin signaling and changes in histone acetylation.

作者信息

Inaba Junichi, McConnell Elizabeth J, Davis Keith R

机构信息

Owensboro Cancer Research Program, Mitchell Memorial Cancer Center, Owensboro, KY 42303, USA.

出版信息

Int J Mol Sci. 2014 Dec 18;15(12):23705-24. doi: 10.3390/ijms151223705.

DOI:10.3390/ijms151223705
PMID:25530619
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4284788/
Abstract

Lunasin is a plant derived bioactive peptide with both cancer chemopreventive and therapeutic activity. We recently showed lunasin inhibits non-small cell lung cancer (NSCLC) cell proliferation in a cell-line-specific manner. We now compared the effects of lunasin treatment of lunasin-sensitive (H661) and lunasin-insensitive (H1299) NSCLC cells with respect to lunasin uptake, histone acetylation and integrin signaling. Both cell lines exhibited changes in histone acetylation, with H661 cells showing a unique increase in H4K16 acetylation. Proximity ligation assays demonstrated lunasin interacted with integrins containing αv, α5, β1 and β3 subunits to a larger extent in the H661 compared to H1299 cells. Moreover, lunasin specifically disrupted the interaction of β1 and β3 subunits with the downstream signaling components phosphorylated Focal Adhesion Kinase (pFAK), Kindlin and Intergrin Linked Kinase in H661 cells. Immunoblot analyses demonstrated lunasin treatment of H661 resulted in reduced levels of pFAK, phosphorylated Akt and phosphorylated ERK1/2 whereas no changes were observed in H1299 cells. Silencing of αv expression in H661 cells confirmed signaling through integrins containing αv is essential for proliferation. Moreover, lunasin was unable to further inhibit proliferation in αv-silenced H661 cells. This indicates antagonism of integrin signaling via αv-containing integrins is an important component of lunasin's mechanism of action.

摘要

芦那辛是一种源自植物的生物活性肽，具有癌症化学预防和治疗活性。我们最近发现芦那辛以细胞系特异性方式抑制非小细胞肺癌（NSCLC）细胞增殖。我们现在比较了芦那辛处理对芦那辛敏感（H661）和芦那辛不敏感（H1299）NSCLC细胞在芦那辛摄取、组蛋白乙酰化和整合素信号传导方面的影响。两种细胞系均表现出组蛋白乙酰化的变化，其中H661细胞显示H4K16乙酰化有独特增加。邻近连接分析表明，与H1299细胞相比，芦那辛在H661细胞中与含有αv、α5、β1和β3亚基的整合素相互作用的程度更大。此外，芦那辛在H661细胞中特异性破坏了β1和β3亚基与下游信号成分磷酸化粘着斑激酶（pFAK）、Kindlin和整合素连接激酶的相互作用。免疫印迹分析表明，用芦那辛处理H661细胞导致pFAK、磷酸化Akt和磷酸化ERK1/2水平降低，而在H1299细胞中未观察到变化。H661细胞中αv表达的沉默证实通过含有αv的整合素进行信号传导对增殖至关重要。此外，芦那辛无法进一步抑制αv沉默的H661细胞的增殖。这表明通过含αv的整合素对整合素信号传导的拮抗作用是芦那辛作用机制的重要组成部分。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbe8/4284788/32431124ed7c/ijms-15-23705-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbe8/4284788/7e46db8b7b1d/ijms-15-23705-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbe8/4284788/d1229795c774/ijms-15-23705-g002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbe8/4284788/3f1a9b5b9b19/ijms-15-23705-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbe8/4284788/0ac80ddc94f7/ijms-15-23705-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbe8/4284788/32431124ed7c/ijms-15-23705-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbe8/4284788/7e46db8b7b1d/ijms-15-23705-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbe8/4284788/d1229795c774/ijms-15-23705-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbe8/4284788/04f44e7fd6ac/ijms-15-23705-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbe8/4284788/3d27fd6d95d6/ijms-15-23705-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbe8/4284788/3f1a9b5b9b19/ijms-15-23705-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbe8/4284788/0ac80ddc94f7/ijms-15-23705-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbe8/4284788/32431124ed7c/ijms-15-23705-g007.jpg

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