Up-regulation of plakophilin-2 is correlated with the progression of glioma

被引:13
|
作者
Zhang, Degeng [1 ]
Qian, Yuxia [2 ]
Liu, Xiaoxing [1 ]
Yu, Hong [3 ]
Zhao, Niangao [4 ]
Wu, Zhengdong [2 ]
机构
[1] Taizhou Peoples Hosp, Dept Oncol, Taizhou, Peoples R China
[2] Taizhou Peoples Hosp, Dept Hematol, 399 Hailing Rd, Taizhou 225300, Jiangsu, Peoples R China
[3] Taizhou Peoples Hosp, Dept Pathol, Taizhou, Peoples R China
[4] Taizhou Peoples Hosp, Dept Neurol, Taizhou, Peoples R China
关键词
glioma; migration; PKP2; proliferation; up-regulation; GROWTH-FACTOR RECEPTOR; TUMOR-CELLS; EXPRESSION; ACTIVATION; THERAPY; BEVACIZUMAB; JUNCTIONS; PROTEINS; CANCERS; PLAQUE;
D O I
10.1111/neup.12363
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Glioma is the most common type of primary brain tumor in the CNS. Due to its poor prognosis and high mortality rates, it is urgent to find outmore effective therapies. Plakophilin-2 (PKP2) is a widespread desmosomal plaque protein. Recently, the important roles of PKP2 in the proliferation and migration of cancer cells and tumor progression has been shown. However, the expression and potential function of PKP2 in glioma was still unclear. In this study, we demonstrated that PKP2 protein expression level was increased in glioma tissues compared with normal brain tissues, and its level was significantly associated with the Ki-67 expression and WHO grade by Western blot analysis and immunohistochemistry. Clinically, high PKP2 expression was tightly related to poor prognosis of glioma patients. Interestingly, we found that down-regulated PKP2 expression was shown to inhibit the migration of cells in glioma. Moreover, cell counting kit (CCK)-8 and colony formation analyses proved that reduced expression of PKP2 could weaken glioma cell proliferation. Taken together, these data uncover a potential role for PKP2 in the pathogenic process of glioma, suggesting that PKP2 may be a promising therapeutic target of glioma.
引用
收藏
页码:207 / 216
页数:10
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