Keratin 19 maintains E-cadherin localization at the cell surface and stabilizes cell-cell adhesion of MCF7 cells.

IF 4.3 3区 材料科学 Q1 ENGINEERING, ELECTRICAL & ELECTRONIC
Sarah Alsharif, Pooja Sharma, Karina Bursch, Rachel Milliken, Van Lam, Arwa Fallatah, Thuc Phan, Meagan Collins, Priya Dohlman, Sarah Tiufekchiev, Georges Nehmetallah, Christopher B Raub, Byung Min Chung
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引用次数: 0

Abstract

A cytoskeletal protein keratin 19 (K19) is highly expressed in breast cancer but its effects on breast cancer cell mechanics are unclear. In MCF7 cells where K19 expression is ablated,we found that K19 is required to maintain rounded epithelial-like shape and tight cell-cell adhesion. A loss of K19 also lowered cell surface E-cadherin levels. Inhibiting internalization restored cell-cell adhesion of KRT19  knockout cells, suggesting that E-cadherin internalization contributed to defective adhesion. Ultimately, while K19 inhibited cell migration and invasion, it was required for cells to form colonies in suspension. Our results suggest that K19 stabilizes E-cadherin complexes at the cell membrane to maintain cell-cell adhesion which inhibits cell invasiveness but provides growth and survival advantages for circulating tumor cells.

角蛋白 19 可维持 E-cadherin 在细胞表面的定位,并稳定 MCF7 细胞的细胞间粘附性。
细胞骨架蛋白角蛋白 19(K19)在乳腺癌中高度表达,但其对乳腺癌细胞力学的影响尚不清楚。在消减 K19 表达的 MCF7 细胞中,我们发现 K19 是维持圆形上皮样形状和细胞间紧密粘附所必需的。K19 的缺失也降低了细胞表面 E-cadherin 的水平。抑制内化可恢复 KRT19 基因敲除细胞的细胞-细胞粘附性,这表明 E-cadherin 内化导致了粘附性缺陷。最终,虽然K19抑制了细胞迁移和侵袭,但细胞在悬浮液中形成菌落却需要它。我们的研究结果表明,K19能稳定细胞膜上的E-cadherin复合物,维持细胞与细胞之间的粘附性,从而抑制细胞的侵袭性,但为循环肿瘤细胞提供生长和存活优势。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
7.20
自引率
4.30%
发文量
567
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