CAP1 is overexpressed in human epithelial ovarian cancer and promotes cell proliferation.
CAP1 is overexpressed in human epithelial ovarian cancer and promotes cell proliferation.
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CAP1在人类上皮卵巢癌中过表达,并促进细胞增殖。
DOI:
10.3892/ijmm.2015.2089
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发表时间:
2015-04
影响因子:
5.4
通讯作者:
Zhong J
中科院分区:
文献类型:
--
作者:
Hua M;Yan S;Deng Y;Xi Q;Liu R;Yang S;Liu J;Tang C;Wang Y;Zhong J
Adenylate cyclase-associated protein 1 (CAP1) regulates both actin filaments and the Ras/cAMP pathway in yeast, and has been found play a role in cell motility and in the development of certain types of cancer. In the present study, we investigated CAP1 gene expression in human epithelial ovarian cancer (EOC). Western blot analysis and immunohistochemistry were performed using EOC tissue samples and the results revealed that CAP1 expression increased with the increasing grade of EOC. In the normal ovarian tissue samples however, CAP1 expression was barely detected. Using Pearson’s χ2 test, it was demonstrated that CAP1 expression was associated with the histological grade and Ki-67 expression. Kaplan-Meier analysis revealed that a higher CAP1 expression in patients with EOC was associated with a poorer prognosis. In in vitro experiments using HO-8910 EOC cells, the expression of CAP1 was knocked down using siRNA. The proliferation of the HO-8910 cells was then determined by cell cycle analysis and cell proliferation assay using the cell counting kit-8 and flow cytometry. The results revealed that the loss of CAP1 expression inhibited cell cycle progression. These findings suggest that a high expression of CAP1 is involved in the pathogenesis of EOC, and that the downregulation of CAP1 in tumor cells may be a therapeutic target for the treatment of patients with EOC.
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影响因子:
2.4
作者:
Li, Mei;Yang, Xiaojing;Zhang, Jianguo
通讯作者:
Zhang, Jianguo
影响因子:
5.3
作者:
MATVIW, H;YU, G;YOUNG, D
通讯作者:
YOUNG, D
影响因子:
3.5
作者:
SWISTON, J;HUBBERSTEY, A;YOUNG, D
通讯作者:
YOUNG, D
影响因子:
64.5
作者:
VOJTEK, A;HAARER, B;WIGLER, M
通讯作者:
WIGLER, M
影响因子:
5
作者:
Yamazaki, Ken;Takamura, Masaaki;Sakamoto, Michiie
通讯作者:
Sakamoto, Michiie