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Mechanisms, Hallmarks, and Implications of Stem Cell Quiescence.干细胞静止的机制、特征及意义。
Stem Cell Reports. 2019 Jun 11;12(6):1190-1200. doi: 10.1016/j.stemcr.2019.05.012.
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EphA8 acts as an oncogene and contributes to poor prognosis in gastric cancer via regulation of ADAM10.EphA8 通过调节 ADAM10 作为癌基因促进胃癌不良预后。
J Cell Physiol. 2019 Nov;234(11):20408-20419. doi: 10.1002/jcp.28642. Epub 2019 Apr 26.
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Cancer statistics, 2019.癌症统计数据，2019 年。
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EphA8 is a Prognostic Factor for Oral Tongue Squamous Cell Carcinoma.EphA8 是口腔舌鳞癌的预后因素。
Med Sci Monit. 2018 Oct 9;24:7213-7222. doi: 10.12659/MSM.910909.
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The Wnt/β-catenin and PI3K/Akt signaling pathways promote EMT in gastric cancer by epigenetic regulation via H3 lysine 27 acetylation.Wnt/β-连环蛋白和PI3K/Akt信号通路通过H3赖氨酸27乙酰化的表观遗传调控促进胃癌中的上皮-间质转化。
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EphA5 and EphA7 forward signaling enhances human hematopoietic stem and progenitor cell maintenance, migration, and adhesion via Rac1 activation.EphA5和EphA7正向信号传导通过激活Rac1增强人类造血干细胞和祖细胞的维持、迁移及黏附。
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EPHA7 and EPHA10 Physically Interact and Differentially Co-localize in Normal Breast and Breast Carcinoma Cell Lines, and the Co-localization Pattern Is Altered in EPHB6-expressing MDA-MB-231 Cells.EPHA7和EPHA10在正常乳腺及乳腺癌细胞系中发生物理相互作用且存在差异共定位，并且在表达EPHB6的MDA-MB-231细胞中，共定位模式发生改变。
Cancer Genomics Proteomics. 2016;13(5):359-68.
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EphA8 is a prognostic marker for epithelial ovarian cancer.EphA8是上皮性卵巢癌的一个预后标志物。
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Identification and Validation of Housekeeping Genes for Gene Expression Analysis of Cancer Stem Cells.用于癌症干细胞基因表达分析的管家基因的鉴定与验证
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侵袭性乳腺癌细胞系 MDA-MB-231 中的干细胞样细胞表达一组独特的 Eph 受体和 Ephrin 配体。

Stem-like Cells from Invasive Breast Carcinoma Cell Line MDA-MB-231 Express a Distinct Set of Eph Receptors and Ephrin Ligands.

机构信息

Department of Basic Medical Sciences, Western University of Health Sciences, Pomona, CA, U.S.A.

出版信息

Cancer Genomics Proteomics. 2020 Nov-Dec;17(6):729-738. doi: 10.21873/cgp.20227.

DOI:10.21873/cgp.20227
PMID:33099474
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7675649/
Abstract

BACKGROUND/AIM: Breast cancer cell lines consist of bulk tumor cells and a small proportion of stem-like cells. While the bulk cells are known to express a distinct combination of Eph receptors and ephrin ligands, the transcript profiles of stem-like cells in these cell lines have not been adequately characterized. The aim of this study was to determine Eph receptor/ephrin ligand profiles of cancer stem cells specific to a triple negative breast carcinoma cell line.

MATERIALS AND METHODS

The normal breast cell line MCF10A and the invasive breast carcinoma cell line MDA-MB-231 were used to isolate CD24/CD24 cell populations. The profiles of Eph receptors and ephrin ligands were determined by real-time PCR and the relative abundance in bulk and stem cells were compared.

RESULTS

Based on the mean ΔCT values, the descending order of abundance was as follows. Ephrin-A5 > EPHA2 > (EPHA8, EPHB2) > ephrin-B2 > (EPHA7, EPHB4, ephrin-A4) > ephrin-A3 > ephrin-A1 > (EPHB3, ephrin-B1) > EPHA4 > EPHA1 > EPHA10. EPHA6 and ephrin-A2 transcripts were not detectable in stem cells from either cell line. The expression of EPHA4, EPHA7, EPHA8, and ephrin-A5 in MDA-MB-231 stem cells was up-regulated by 12, 20, ~500, and 6.5-fold respectively.

CONCLUSION

The up-regulation of transcripts for EPHA8 and its cognate ligand, ephrin-A5, in the stem cells isolated from MDA-MB-231, suggest their involvement in the invasiveness of this cell line. Based on literature reports, we propose the role of EPHA8 and ephrin-A5 in MDA-MB-231 stem cells via the PI3K-AKT-mTOR pathway.

摘要

背景/目的：乳腺癌细胞系由大量肿瘤细胞和一小部分干细胞样细胞组成。尽管已知大量细胞表达独特的 Eph 受体和 Ephrin 配体组合，但这些细胞系中干细胞样细胞的转录谱尚未得到充分表征。本研究旨在确定特定于三阴性乳腺癌细胞系的癌症干细胞的 Eph 受体/Ephrin 配体谱。

材料和方法

使用正常乳腺细胞系 MCF10A 和侵袭性乳腺癌细胞系 MDA-MB-231 分离 CD24/CD24 细胞群。通过实时 PCR 确定 Eph 受体和 Ephrin 配体的图谱，并比较大量细胞和干细胞中的相对丰度。

结果

基于平均 ΔCT 值，丰度的降序如下。Ephrin-A5>EPHA2>（EPHA8、EPHB2）>ephrin-B2>（EPHA7、EPHB4、ephrin-A4）>ephrin-A3>ephrin-A1>（EPHB3、ephrin-B1）>EPHA4>EPHA1>EPHA10。来自两种细胞系的干细胞中均未检测到 EPHA6 和 ephrin-A2 转录本。EPHA4、EPHA7、EPHA8 和 ephrin-A5 在 MDA-MB-231 干细胞中的表达分别上调了 12、20、~500 和 6.5 倍。

结论

从 MDA-MB-231 中分离的干细胞中 Ephrin-A5 的上调及其同源配体 EPHA8 的上调表明它们参与了该细胞系的侵袭性。根据文献报道，我们提出了 EPHA8 和 ephrin-A5 在 MDA-MB-231 干细胞中通过 PI3K-AKT-mTOR 途径发挥作用。