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首页> 外文期刊>Journal of cellular physiology. >CXCL3 overexpression promotes the tumorigenic potential of uterine cervical cancer cells via the MAPK/ERK pathway
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CXCL3 overexpression promotes the tumorigenic potential of uterine cervical cancer cells via the MAPK/ERK pathway

机译：CXCL3超表达促进了肿瘤发生的通过子宫宫颈癌细胞的潜力MAPK / ERK通路

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摘要

CXCL3 belongs to the CXC-type chemokine family and is known to play a multifaceted role in various human malignancies. While its clinical significance and mechanisms of action in uterine cervical cancer (UCC) remain unclear. This investigation demonstrated that the UCC cell line HeLa expressed CXCL3, and strong expression of CXCL3 was detected in UCC tissues relative to nontumor tissues. In addition, CXCL3 expression was strongly correlated with CXCL5 expression in UCC tissues. In vitro, HeLa cells overexpressing CXCL3, HeLa cells treated with exogenous CXCL3 or treated with conditioned medium from WPMY cells overexpressing CXCL3, exhibited enhanced proliferation and migration activities. In agreement with these findings, CXCL3 overexpression was also associated with the generation of HeLa cell tumor xenografts in athymic nude mice. Subsequent mechanistic studies demonstrated that CXCL3 overexpressing influenced the expression of extracellular signal-regulated kinase (ERK) signaling pathway associated genes, including ERK1/2, Bcl-2, and Bax, whereas the CXCL3-induced proliferation and migration effects were attenuated by exogenous administration of the ERK1/2 blocker PD98059. The data of the current investigation support that CXCL3 appears to hold promise as a potential tumor marker and interference target for UCC.
机译：CXCL3属于CXC-type趋化因子家族众所周知,各发挥多方面的作用人类恶性肿瘤。意义和子宫中作用的机制宫颈癌(UCC)尚不清楚。调查表明,UCC细胞系海拉表示CXCL3,强烈的表达CXCL3中检测出UCC组织相对于nontumor组织。有密切关系CXCL5表达吗UCC组织。CXCL3,海拉细胞与外生CXCL3或治疗处理从WPMY细胞条件培养基overexpressing CXCL3,表现出增强的增殖和迁移活动。同意这些发现,CXCL3超表达也是相关的代的海拉细胞肿瘤异种移植无胸腺的裸小鼠。证明CXCL3 overexpressing影响细胞外signal-regulated的表达激酶(ERK)信号通路相关基因,包括ERK1/2、bcl - 2,和伯灵顿,而CXCL3-induced增殖和迁移的影响减毒的外生政府吗ERK1/2阻滞剂PD98059。目前调查支持CXCL3出现承诺作为一个潜在的肿瘤标记干扰UCC的目标。

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