Bmi1 drives stem-like properties and is associated with migration, invasion, and poor prognosis in tongue squamous cell carcinoma.
Bmi1 drives stem-like properties and is associated with migration, invasion, and poor prognosis in tongue squamous cell carcinoma.
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Bmi1 驱动干细胞样特性，并与舌鳞状细胞癌的迁移、侵袭和不良预后相关。
DOI：
10.7150/ijbs.10405
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发表时间：
2015
影响因子：
9.2
通讯作者：
Wang A
中科院分区：
文献类型：
--
作者：
He Q;Liu Z;Zhao T;Zhao L;Zhou X;Wang A
Bmi 1（B细胞特异性莫洛尼鼠白血病病毒插入位点1）参与干细胞的自我更新和多种恶性肿瘤的发生。本研究旨在探讨Bmi 1在舌鳞状细胞癌（TSCC）发生发展中的作用及其对TSCC迁移和侵袭的影响。最初，免疫组化显示Bmi 1过表达是癌前异型增生、原发性TSCC和淋巴结转移的常见事件，并且与不良预后相关。Bmi 1和SOD 2（锰超氧化物歧化酶）表达之间存在显著相关性。侧群（SP）细胞用作癌症干细胞样细胞，并通过球体和集落形成测定以及干细胞标志物的表达进一步评估。具有较高迁移和侵袭能力的TSCC细胞（UM 1细胞系）显示出较高比例的SP细胞和Bmi 1表达，而具有较低迁移和侵袭能力的TSCC细胞（UM 2细胞系）显示出较高比例的SP细胞和Bmi 1表达。在UM 1或SP细胞中敲低Bmi 1抑制迁移和侵袭，并减少球体和集落形成，以及干细胞标志物和SOD 2的表达。通过染色质免疫沉淀和荧光素酶测定证明C-myc与Bmi 1启动子的直接结合。此外，C-myc基因的敲低抑制SP细胞的迁移和侵袭，并降低Bmi 1和SOD 2的表达。我们的研究结果表明，Bmi 1表达失调是一个常见的事件在发展过程中的TSCC，并可能有预后价值的患者与这种疾病。Bmi 1介导的TSCC迁移和侵袭与肿瘤干细胞样细胞有关，涉及C-myc-Bmi 1-SOD 2通路。
Bmi1 (B-cell-specific Moloney murine leukemia virus insertion site 1) had been found to involve in self -renewal of stem cells and tumorigenesis in various malignancies. The purpose of this study is to evaluate the role of Bmi1 in the development of tongue squamous cell carcinoma (TSCC) and its functional effect on the migration and invasion of TSCC. Initially, immunohistochemistry revealed that Bmi1 overexpression was a common event in premalignant dysplasia, primary TSCC, and lymph node metastases and was associated with a poor prognosis. A significant correlation between Bmi1 and SOD2 (manganese superoxide dismutase) expression was observed. Side population (SP) cells were used as cancer stem-like cells and further assessed by sphere and colony formation assays, and the expression of stem cell markers. TSCC cells with higher migration and invasion ability (UM1 cell lines) showed a higher proportion of SP cells and Bmi1 expression than TSCC cells with lower migration and invasion ability (UM2 cell lines). Knockdown of Bmi1 in UM1 or SP cells inhibited migration and invasion and decreased the sphere and colony formation, and the expression of stem cell markers and SOD2. Direct binding of C-myc to the Bmi1 promoter was demonstrated by chromatin immunoprecipitation and luciferase assays. Moreover, C-myc knockdown in SP cells inhibited their migration and invasion and decreased the expression of Bmi1 and SOD2. Our results indicate that the deregulation of Bmi1 expression is a frequent event during the progression of TSCC and may have a prognostic value for patients with this disease. The Bmi1-mediated migration and invasion of TSCC is related to cancer stem-like cells and involves the C-myc-Bmi1-SOD2 pathway.
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影响因子：
3.3
作者：
Feng, Jin-Qiu;Xu, Zi-Yuan;Zhou, Zeng-Tong
通讯作者：
Zhou, Zeng-Tong
癌蛋白 Bmi-1 通过激活 IKK-核因子-kappaB 通路，对神经胶质瘤细胞产生凋亡抵抗。
影响因子：
6
作者：
Li, Jun;Gong, Li-Yun;Li, Mengfeng
通讯作者：
Li, Mengfeng
影响因子：
4.8
作者：
Chen, Hui;Zhou, Liang;Tian, Jie
通讯作者：
Tian, Jie
影响因子：
3.2
作者：
Lim, Wonbong;Choi, Hongran;Kim, Okjoon
通讯作者：
Kim, Okjoon
影响因子：
6.6
作者：
Ding X;Zhang N;Cai Y;Li S;Zheng C;Jin Y;Yu T;Wang A;Zhou X
通讯作者：
Zhou X