HEPACAM inhibited the growth and migration of cancer cells in the progression of non-small cell lung cancer

被引:6
|
作者
Shao, Huanzhang [1 ]
Gu, Yinjie [2 ]
Ding, Junli [3 ]
Lu, Peihua [3 ]
Ruan, Tingyan [3 ]
Lu, Wenbin [4 ]
机构
[1] Zhengzhou Univ, Henan Prov Peoples Hosp, Dept Crit Care Med, Zhengzhou 450003, Peoples R China
[2] Jiangsu Univ, Affiliated Yixing Peoples Hosp, Dept Crit Care Med, Yixing 214200, Jiangsu, Peoples R China
[3] Nanjing Med Univ, Dept Med Oncol, Wuxi Peoples Hosp, Wuxi 214023, Jiangsu, Peoples R China
[4] Jiangsu Univ, Dept Med Oncol, Wujin Peoples Hosp, 2 North Yongning Rd, Changzhou 213002, Jiangsu, Peoples R China
关键词
HEPACAM; Non-small cell lung cancer; Cell growth and migration; Beta-catenin/TCF; ADHESION MOLECULE HEPACAM; E-CADHERIN; EXPRESSION; CATENIN; GENE; CARCINOMA; TRANSLOCATION;
D O I
10.1007/s13277-015-4084-9
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Hepatocyte cell adhesion molecule (HEPACAM), a member of immunoglobulin superfamily, is an adhesion molecule. Although dysregulation of several adhesion molecules has been implicated in the progression of non-small cell lung cancer (NSCLC), the expression profile and functions of HEPACAM in NSCLC remains unknown. In this study, it was found that the expression of HEPACAM was downregulated in NSCLC tissues. Forced expression of HEPACAM in NSCLC cells inhibited the growth and migration of the cancer cells, while knocking down the expression of HEPACAM promoted cell growth, migration, and metastasis. In the molecular mechanism study, HEPACAM was found to be a negative regulator of beta-catenin/TCF signaling. Taken together, this study revealed the suppressive roles of HEPACAM in NSCLC and restoring the function of HEPACAM in NSCLC might be a promising strategy for the therapy.
引用
收藏
页码:2621 / 2627
页数:7
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