Ets-1在纤连蛋白衍生的肝素结合域多肽减轻黑色素瘤细胞侵袭性和化疗耐药性中的作用。

Role of Ets-1 in fibronectin-derived heparin-binding domain polypeptides alleviating melanoma cell invasiveness and chemoresistance.

作者信息

Tang Nanhong, Wang Xiaoqian, Huang Tao, Wu Yong, Chen Yuanzhong

机构信息

Fujian Institute of Hepatobiliary Surgery, Fujian Medical University Union Hospital, Fuzhou, China.

出版信息

Exp Dermatol. 2014 Jul;23(7):512-3. doi: 10.1111/exd.12444.

DOI:10.1111/exd.12444

PMID:24816403

Abstract

In this study, we observed that rhFNHN29 and rhFNHC36, two recombinant heparin-binding domain polypeptides of fibronectin, suppressed adhesion and invasion of B16F10 and A375 melanoma cells mediated by integrin αv and α2 in a dose-dependent manner. Combined with low-concentration epirubicin (EPI), rhFNHN29 or rhFNHC36 exhibited a synergistic inhibition on the viability and metastasis of B16F10 cells. Moreover, in the presence of high-concentration rhFNHN29 or rhFNHC36, the Ets-1 activity and the expression of p-FAK, p-Erk1/2 and Ets-1 were notably downregulated in B16F10 cells. Ets-1 is one of the central regulatory links for rhFNHN29 and rhFNHC36 to suppress the adhesion and invasion of melanoma cells. Combining rhFNHN29 or rhFNHC36 with EPI may be a good way to alleviate invasiveness or chemoresistance in melanoma.

摘要

在本研究中，我们观察到纤连蛋白的两种重组肝素结合域多肽rhFNHN29和rhFNHC36以剂量依赖性方式抑制整合素αv和α2介导的B16F10和A375黑色素瘤细胞的黏附与侵袭。与低浓度表柔比星（EPI）联合使用时，rhFNHN29或rhFNHC36对B16F10细胞的活力和转移表现出协同抑制作用。此外，在高浓度rhFNHN29或rhFNHC36存在的情况下，B16F10细胞中Ets-1活性以及p-FAK、p-Erk1/2和Ets-1的表达显著下调。Ets-1是rhFNHN29和rhFNHC36抑制黑色素瘤细胞黏附与侵袭的核心调控环节之一。将rhFNHN29或rhFNHC36与EPI联合使用可能是减轻黑色素瘤侵袭性或化疗耐药性的一种好方法。