Yang Yang, Hou Jie, Shao Mingliang, Zhang Wei, Qi Yaling, E Shengnan, Wang Shuqiu, Sui Hongyu, Meng Dexin, Wang Baixin, Wang Mingfu, Han Yang, Cao Yu, Huang Xiaoqing, Li Yue, Zhang Pengxia, Wang Weiqun
Basic Medical College, Jiamusi University, Jiamusi, Heilongjiang 154007, P.R. China.
The First Affiliated Hospital, Jiamusi University, Jiamusi, Heilongjiang 154002, P.R. China.
Oncol Lett. 2017 Dec;14(6):7977-7985. doi: 10.3892/ol.2017.7236. Epub 2017 Oct 20.
C-X-C motif chemokine ligand 5 (CXCL5) is a CXC-type chemokine that is a crucial inflammatory mediator and a powerful attractant for granulocytic immune cells. Increasing evidence has indicated that CXCL5 is involved in the tumorigenesis of various malignancies. The present investigation demonstrated that CXCL5 was expressed in both hepatoblastoma HepG2 cells and liver stellate LX-2 cells, and CXCL5's receptor C-X-C chemokine receptor type 2 (CXCR2) was expressed in HepG2 cells by reverse transcription-polymerase chain reaction (RT-PCR), western blotting and ELISA assays. Cell counting kit-8, colony formation and Transwell assays revealed that exogenous CXCL5 expression efficiently promoted proliferation, colony formation and migration of HepG2 cells. To explore the autocrine and paracrine roles of CXCL5 in the oncogenic potential of HepG2 cells, HepG2 cells overexpressing CXCL5 and LX-2 cells overexpressing CXCL5 were successfully constructed by gene transfection. Similarly, overexpression of CXCL5 in HepG2 also enhanced proliferation, colony formation and migration of HepG2 cells. Furthermore, the condition medium of LX-2 cells overexpressing CXCL5 affected the proliferation and migration of HepG2 cells. RT-PCR and western blotting assays were also conducted to explore whether overexpression of CXCL5 in HepG2 modulated the expression of genes. The results revealed that overexpression of CXCL5 regulated the expression of several genes, including N-myc downregulated gene 3,w B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein, P53, vascular endothelial growth factor, interleukin (IL)-18, IL-1β and cystathionine-γ-lyase. In conclusion, the present findings indicate that CXCL5/CXCR2 axis contributes to the oncogenic potential of hepatoblastoma via autocrine or paracrine pathways by regulating expression of genes associated with the progression of carcinoma.
C-X-C基序趋化因子配体5（CXCL5）是一种CXC型趋化因子，是一种关键的炎症介质，也是粒细胞免疫细胞的强大趋化剂。越来越多的证据表明，CXCL5参与了各种恶性肿瘤的发生。本研究表明，CXCL5在肝母细胞瘤HepG2细胞和肝星状LX-2细胞中均有表达，通过逆转录聚合酶链反应（RT-PCR）、蛋白质印迹法和酶联免疫吸附测定（ELISA）检测发现，CXCL5的受体C-X-C趋化因子受体2（CXCR2）在HepG2细胞中有表达。细胞计数试剂盒-8、集落形成和Transwell实验表明，外源性CXCL5表达有效地促进了HepG2细胞的增殖、集落形成和迁移。为了探究CXCL5在HepG2细胞致癌潜能中的自分泌和旁分泌作用，通过基因转染成功构建了过表达CXCL5的HepG2细胞和过表达CXCL5的LX-2细胞。同样，HepG2细胞中CXCL5的过表达也增强了HepG2细胞的增殖、集落形成和迁移。此外，过表达CXCL5的LX-2细胞的条件培养基影响了HepG2细胞的增殖和迁移。还进行了RT-PCR和蛋白质印迹分析，以探究HepG2细胞中CXCL5的过表达是否调节基因表达。结果显示，CXCL5的过表达调节了多个基因的表达，包括N-myc下调基因3、B细胞淋巴瘤-2（Bcl-2）、Bcl-2相关X蛋白、P53、血管内皮生长因子、白细胞介素（IL）-18、IL-1β和胱硫醚-γ-裂解酶。总之，本研究结果表明，CXCL5/CXCR2轴通过调节与癌进展相关基因的表达，通过自分泌或旁分泌途径促进肝母细胞瘤的致癌潜能。
