First Department of Pediatrics, First Affiliated Hospital of Jiamusi University, Jiamusi 154002, Heilongjiang, P.R China.
Department of Gastroenterology, Affiliated Hospital of Inner Mongolia Medical University, Hohhot 010050, Inner Mongolia, P.R China.
Biosci Rep. 2020 Aug 28;40(8). doi: 10.1042/BSR20201169.
CXCL8, a member of CXC chemokines, was constitutively expressed in many types of human cancers, and its overexpression has been shown to play a critical role in promoting tumorigenesis. The purpose of the present study was to determine CXCL8 expression in a commercial human liver tissue microarray, and elucidate the effects and underlying mechanisms by which CXCL8 is involved in the malignant progression of human liver cancer. Our data showed that high level expression of CXCL8 in tissues with liver cancer was identified as compared with non-cancer tissues, and its up-regulation was closely associated with clinical stage and tumor infiltration. In vitro, exogenous CXCL8 at concentrations of 10, 20 or 40 ng/ml obviously stimulated the proliferation abilities of HepG2 cells. Coupled with this, 10, 20 or 40 ng/ml of exogenous CXCL8 also triggered a significant elevation in HepG2 cells migration. Additionally, overexpression of CXCL8 in HepG2 cells also resulted in increased cell proliferation and migration capacities. Finally, Western blotting analysis showed that overexpression of CXCL8 increased the expression of ERK, p-ERK and survivin, decreased the expression of caspase-3 and BAX at protein level.
CXCL8，一种属于 CXC 趋化因子的成员，在许多类型的人类癌症中持续表达，其过表达已被证明在促进肿瘤发生中起着关键作用。本研究的目的是确定 CXCL8 在商业性人类肝脏组织微阵列中的表达，并阐明 CXCL8 参与人类肝癌恶性进展的作用和潜在机制。我们的数据表明，与非癌组织相比，肝癌组织中 CXCL8 的高表达被鉴定为高表达，其上调与临床分期和肿瘤浸润密切相关。在体外，浓度为 10、20 或 40ng/ml 的外源性 CXCL8 明显刺激 HepG2 细胞的增殖能力。与此相关的是，10、20 或 40ng/ml 的外源性 CXCL8 也引发 HepG2 细胞迁移的显著增加。此外，CXCL8 在 HepG2 细胞中的过表达也导致细胞增殖和迁移能力的增加。最后，Western blot 分析表明，CXCL8 的过表达增加了 ERK、p-ERK 和 survivin 的表达，降低了 caspase-3 和 BAX 的表达。
