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首页> 外文期刊>Life sciences >Tumor suppressor carcinoembryonic antigen-related cell adhesion molecule 1 potentates the anchorage-independent growth of human hepatoma HepG2 cells.
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Tumor suppressor carcinoembryonic antigen-related cell adhesion molecule 1 potentates the anchorage-independent growth of human hepatoma HepG2 cells.

机译：肿瘤抑制癌胚抗原相关细胞粘附分子1增强了人肝癌HepG2细胞的锚定非依赖性生长。

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摘要

Carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1), an adhesion molecule of the immunoglobulin superfamily, has been characterized as a putative tumor suppressor because it is frequently down-regulated in aggressive types of cancer cells. Recently, however, several studies have shown that CEACAM1 actively contributes to malignant progression or migration in some types of tumor cells, suggesting that the role of CEACAM1 might be diverse among different types of cancer cells. To investigate the functional consequences of CEACAM1 expression in hepatocellular carcinoma, we analyzed the status of CEACAM1 in hepatoma cell lines HLF, PLC/PRF/5, HepG2 and KYN-2. We found that CEACAM1 was only expressed in HepG2 cells, which show a unique property for enhanced anchorage-independent growth. When HepG2 cells were treated with small interfering RNA targeted against CEACAM1, the growth rate in monolayer culture was increased. In contrast, when HepG2 cells were cultured in suspension, inhibition of CEACAM1 expression significantly decreased the growth rate, and the speed of cell-cell attachment was repressed. Hyaluronidase treatment attenuated the growth rate of HepG2 cells in suspension culture, indicating that cell-cell attachment is a requisite for anchorage-independent growth. Our data may reveal the dual role of CEACAM1 on hepatocarcinogenesis, by showing that CEACAM1 acts as a tumor suppressor in HepG2 cells in anchorage-dependent growth conditions, while in anchorage-independent growth conditions, it augments cell proliferation by potentiating the cell-cell attachment.
机译：癌胚抗原相关细胞粘附分子1（CEACAM1）是免疫球蛋白超家族的粘附分子，由于其在侵略性类型的癌细胞中经常被下调，因此被认为是公认的肿瘤抑制因子。然而，最近，一些研究表明，CEACAM1在某些类型的肿瘤细胞中积极地促进了恶性进展或迁移，表明CEACAM1的作用在不同类型的癌细胞中可能是多种多样的。为了研究CEACAM1在肝细胞癌中表达的功能后果，我们分析了CEACAM1在肝癌细胞系HLF，PLC​​ / PRF / 5，HepG2和KYN-2中的状态。我们发现CEACAM1仅在HepG2细胞中表达，其显示出增强的锚定非依赖性生长的独特特性。当用靶向CEACAM1的小干扰RNA处理HepG2细胞时，单层培养物中的生长速率增加。相反，当悬浮培养HepG2细胞时，对CEACAM1表达的抑制作用显着降低了生长速率，并抑制了细胞与细胞的附着速度。透明质酸酶处理可减缓悬浮培养中HepG2细胞的生长速率，表明细胞与细胞的附着是锚定非依赖性生长的必要条件。我们的数据可能显示CEACAM1在肝癌发生中的双重作用，方法是显示CEACAM1在锚定依赖性生长条件下在HepG2细胞中起肿瘤抑制作用，而在锚定依赖性生长条件下，它通过增强细胞与细胞的附着来增强细胞增殖。 。

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