Expression of Nischarin negatively correlates with estrogen receptor and alters apoptosis, migration and invasion in human breast cancer
Expression of Nischarin negatively correlates with estrogen receptor and alters apoptosis, migration and invasion in human breast cancer
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Nischarin 的表达与雌激素受体负相关并改变人乳腺癌的细胞凋亡、迁移和侵袭
DOI：
10.1016/j.bbrc.2017.01.109
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发表时间：
2017-03-11
影响因子：
3.1
通讯作者：
Zhang, Liling
中科院分区：
文献类型：
--
作者：
Chang, Chan;Wei, Wujie;Zhang, Liling
Nischarin是一种新的整合素结合蛋白，已被证明对细胞迁移和侵袭具有负面作用。然而，Nischarin在乳腺癌中的生物学作用尚未完全阐明。本研究旨在分析Nischarin的表达与乳腺癌患者临床特征的关系，进一步探讨Nischarin在乳腺癌细胞凋亡、迁移和侵袭中的作用。结果显示，Nischarin在乳腺癌组织中的表达(37.8%，23/67)显著低于正常乳腺组织(61.8%，21/34；P<；0.05)，且Nischarin的表达与雌激素受体状态呈显著负相关。进一步的实验表明，Nischarin的过表达可以诱导细胞凋亡，并抑制细胞的迁移和侵袭。目前的研究结果证实Nishcharin可能是一种新的肿瘤抑制因子，在乳腺癌细胞的凋亡和转移中发挥重要作用，可作为乳腺癌治疗的潜在靶点。(C)2017 Elsevier Inc.保留所有权利。
Nischarin, a novel integrin binding protein, has been demonstrated its negative effects on cell migration and invasion. However, the biological role of Nischarin in breast cancer has not been fully elucidated yet. Our study aimed to analyze the association between Nischarin expression and clinical features of breast cancer patients, and further investigate the role of Nischarin in breast cancer cells apoptosis, migration and invasion. Results showed that Nischarin expression was significantly lower in breast cancer tissues (37.8%, 23/67) than in normal tissues (61.8%, 21/34; P < 0.05), and the expression of Nischarin significantly negatively correlated with estrogen receptor status Similarly, Nischarin expression was highest in normal breast cell line HBL-100 while triple-negative breast cancer cell line MDA-MB-231 had the lowest expression of Nischarin. Further experiments demonstrated that overexpression of Nischarin may induce apoptosis, and inhibit cell migration and invasion. The present data confirmed that Nishcharin might be a novel tumor suppressor and plays an important role in breast cancer cell apoptosis and metastasis, which can be used as a potential therapeutic target for breast cancer treatment. (C) 2017 Elsevier Inc. All rights reserved.