Growth factor progranulin contributes to cervical cancer cell proliferation and transformation in vivo and in vitro
Growth factor progranulin contributes to cervical cancer cell proliferation and transformation in vivo and in vitro
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生长因子颗粒体蛋白前体有助于体内外宫颈癌细胞的增殖和转化。
DOI：
10.1016/j.ygyno.2014.05.025
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发表时间：
2014-08-01
影响因子：
4.7
通讯作者：
Tang, Wei
中科院分区：
文献类型：
--
作者：
Lu, Yi;Zheng, Lin;Tang, Wei
Objective.生长因子颗粒蛋白前体（PGRN）在许多肿瘤中过表达。我们的目的是研究PGRN在宫颈癌发生中的表达和作用。通过Western印迹分析、ELISA或免疫组织化学评估细胞和正常和癌性宫颈组织中PGRN的表达和分泌。PGRN在宫颈癌发生中的作用通过细胞增殖、集落形成和肿瘤生长测定来探讨。我们评估了PGRN介导的信号转导在宫颈细胞中的作用。PGRN表达在宫颈癌细胞系和组织中上调。PGRN促进人宫颈上皮H8细胞体外转化和体内成瘤。体内宫颈癌细胞中PGRN表达的敲低降低了细胞增殖并减缓了肿瘤生长。PGRN刺激宫颈细胞增殖，转化至少部分是由Akt和Erk信号介导的。PGRN在宫颈癌中过表达，并促进宫颈细胞的恶性生长和转化。因此，PGRN在宫颈癌的发生中起着关键作用，并显示出对宫颈癌治疗策略的希望。(C)2014爱思唯尔公司All rights reserved.
Objective. The growth factor progranulin (PGRN) is overexpressed in a number of tumors. We aimed to investigate the expression and role of PGRN in cervical cancer tumorigenesis.Methods. PGRN expression and secretion was assessed in cells and normal and cancerous cervical tissues by Western blot analysis, ELISA or immunohistochemistry. The role of PGRN in cervical carcinogenesis was explored by cell-proliferation, colony-formation and tumor-growth assays. We assessed the role of PGRN-mediated signaling in the cervical cell with specific inhibitors.Results. PGRN expression was upregulated in cervical cancer cell lines and tissue. PGRN promoted the transformation of human cervical mucosa epithelial H8 cells in vitro and tumor formation in vivo. Knockdown of PGRN expression in cervical cancer cells in vivo decreased cell proliferation and slowed tumor growth. PGRN stimulated cervical cell proliferation, and transformation was mediated, at least in part, by Akt and Erk signaling.Conclusions. PGRN is overexpressed in cervical cancer and promotes the malignant growth and transformation of cervical cells. Therefore, PGRN plays a critical role in carcinogenesis of cervical cancer and shows promise for therapeutic strategies for cervical cancer. (C) 2014 Elsevier Inc. All rights reserved.