The receptor for activated protein kinase C promotes cell growth, invasion and migration in cervical cancer.
The receptor for activated protein kinase C promotes cell growth, invasion and migration in cervical cancer.
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活化蛋白激酶C受体促进宫颈癌细胞生长、侵袭和迁移
DOI：
10.3892/ijo.2017.4137
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发表时间：
2017-11
影响因子：
5.2
通讯作者：
Zhou Y
中科院分区：
文献类型：
--
作者：
Liao S;Xiao S;Chen H;Zhang M;Chen Z;Long Y;Gao L;He J;Ge Y;Yi W;Wu M;Li G;Zhou Y
宫颈癌是全世界女性最常见的恶性肿瘤之一。然而，宫颈癌的确切病因仍不清楚。据报道，活化蛋白激酶 C (RACK1) 的受体参与肿瘤发生和肿瘤进展。此外，RACK1在多种肿瘤中的预后价值已得到确定。然而，关于 RACK1 在宫颈癌中的功能作用的研究有限。在本研究中，我们通过免疫组织化学和蛋白质印迹技术检测了RACK1的表达水平，发现它在宫颈癌中表达上调。集落形成和 CCK8 检测表明 RACK1 促进 CaSki 宫颈癌细胞的细胞增殖。而 CCK8 分析中 RACK1 的沉默会降低细胞增殖。 β-半乳糖苷酶染色表明 RACK1 可以减少宫颈癌细胞的细胞衰老。侵袭和迁移实验表明RACK1促进宫颈癌细胞的侵袭和迁移。此外，当 RACK1 被静音时，它会产生相反的结果。此外，通过 qPCR 分析，RACK1 过表达的 CaSki 细胞中 MMP-3、MMP-9 和 MMP-10 的 mRNA 表达水平上调。 RACK1还在细胞周期分析中诱导S期积累并抑制宫颈癌细胞的细胞凋亡。线粒体功能的流式细胞术分析表明，RACK1 增加线粒体膜电位 (Δψm) 水平，以防止宫颈癌细胞中的线粒体凋亡。为了探讨RACK1的可能机制，我们测试发现RACK1上调宫颈癌细胞中NF-κB、cyclin D1和CDK4的表达，下调p53、p38、p21和STAT1的表达。这些结果表明，RACK1可能通过影响p53通路来促进宫颈癌细胞的生长和侵袭，并抑制衰老和凋亡。
Cervical cancer is one of the most common malignant tumors in women all over the world. However, the exact etiology of cervical cancer remains unclear. The receptor for activated protein kinase C (RACK1) is reported to be involved in tumorigenesis and tumor progression. Besides, the prognostic value of RACK1 in several kinds of tumors has been identified. However, there are limited studies on the functional role of RACK1 in cervical cancer. In this study, we tested the expression level of RACK1 by immunohistochemistry and western blot technologies and find that it is upregulated in cervical cancer. Colony formation and CCK8 assays indicate that RACK1 promotes cell proliferation in CaSki cervical cancer cells. While the silence of RACK1 decreases the cell proliferation in CCK8 analysis. β-galactosidase staining suggests that RACK1 decreases cell senescence in cervical cancer cells. Invasion and migration assay show that RACK1 promotes the invasion and migration of cervical cancer cells. Also, when RACK1 was silenced, it exerts the opposite result. Furthermore, the mRNA expression levels of MMP-3, MMP-9 and MMP-10 were upregulated in RACK1-overexpressed CaSki cells by qPCR analysis. RACK1 also induces S phase accumulation in cell cycle analysis and suppresses cell apoptosis in cervical cancer cells. Flow cytometry analysis of mitochondria functions suggests that RACK1 increases the mitochondrial membrane potential (Δψm) levels to prevent mitochondrial apoptosis in cervical cancer cells. To explore the possible mechanism of RACK1, we tested and found that RACK1 upregulates the expression of NF-κB, cyclin D1 and CDK4 and downregulates the expression of p53, p38, p21 and STAT1 in cervical cancer cells. These results suggest that RACK1 promotes cell growth and invasion and inhibits the senescence and apoptosis in cervical cancer cells probably by affecting the p53 pathway.
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影响因子：
4.3
作者：
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作者：
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