CRKL overexpression suppresses in vitro proliferation, invasion and migration of murine hepatocarcinoma Hca-P cells
CRKL overexpression suppresses in vitro proliferation, invasion and migration of murine hepatocarcinoma Hca-P cells
复制标题
CRKL过表达抑制小鼠肝癌Hca-P细胞的体外增殖、侵袭和迁移
DOI：
10.1016/j.biopha.2014.10.025
复制
发表时间：
2015-02-01
影响因子：
7.5
通讯作者：
Liu, Shuqing
中科院分区：
文献类型：
--
作者：
Lin, Qiuyue;Sun, Ming-Zhong;Liu, Shuqing
CRK家族蛋白在肿瘤细胞的生长、增殖、迁移和侵袭过程中起重要作用。以前，我们发现CRK参与小鼠肝癌细胞的淋巴转移潜能。鸡肿瘤病毒10号激酶样蛋白调节因子（CRKL）是CRK家族的成员之一，与淋巴结转移（LNM）率约为25%的小鼠肝癌细胞Hca-P的恶性行为有关。构建的真核表达载体pcDNA3.1/V5-HisB-CRKL在Hca-P细胞中过表达CRKL可显著改善其恶性生物学特性。CCK-8和软琼脂集落形成实验表明CRKL过表达可显著抑制Hca-P细胞的增殖和集落形成能力，transwell实验表明CRKL过表达可显著降低Hca-P细胞的迁移和侵袭能力。由于Hca-P是一种理想的肝癌细胞模型，具有低（初始）LNM潜力，CRKL被证明是一种潜在的抑制剂，并为肝癌细胞的恶性行为和肝癌的淋巴转移机制提供了新的见解。(C)2014年Elsevier Masson SAS。All rights reserved.
The signal adaptor CRK family protein play important roles in cancer cell progression, proliferation, migration and invasion. Previously, we showed that CRK was involved in lymphatic metastatic potential of murine hepatocarcinoma cells. In current work, as a member of CRK family, chicken tumour virus number 10 regulator of kinase-like protein (CRKL) was revealed to be associated with malignant behaviors of Hca-P, a murine HCC cell with lymph node metastatic (LNM) rate of similar to 25%. CRKL overexpression in Hca-P by a constructed eukaryotic expression vector of pcDNA3.1/V5-HisB-CRKL significantly ameliorated its malignant biological properties. CCK-8 and soft agar colony formation assays indicated CRKL overexpression significantly inhibits the cell proliferation and colony formation abilities of Hca-P. Additionally, transwell assays indicated that the Hca-P cell migration and invasion capacities were apparently reduced following CRKL overexpression. As Hca-P is an ideal hepatocarcinoma cell model with low (initial) LNM potential, CRKL is shown to act as a potential suppressor and to provide new insight for both the malignant behaviors of hepatocarcinoma cells and lymphatic metastasis mechanism of hepatocarcinoma. (C) 2014 Elsevier Masson SAS. All rights reserved.