详细信息
CXCL12和CXCL8调控结肠癌增殖和转移的机制研究 被引量:7
CXCL12 promotes CXCL8 secretion and co-operatively enhance metastatic potential of colon cancer cell lines
文献类型:期刊文献
中文题名:CXCL12和CXCL8调控结肠癌增殖和转移的机制研究
英文题名:CXCL12 promotes CXCL8 secretion and co-operatively enhance metastatic potential of colon cancer cell lines
作者:龚珍强[1];马家驰[2];苏河[2];陈泉[2];杜剑波[1];亓建波[3];赵晓丹[1]
第一作者:龚珍强
机构:[1]宁夏医科大学临床学院研究生院,银川750004;[2]甘肃省人民医院普通外科;[3]甘肃中医药大学研究生院
第一机构:宁夏医科大学临床学院研究生院,银川750004
年份:2018
卷号:33
期号:3
起止页码:244
中文期刊名:中华普通外科杂志
外文期刊名:Chinese Journal of General Surgery
收录:CSTPCD;;北大核心:【北大核心2017】;CSCD:【CSCD_E2017_2018】;
基金:国家自然科学基金资助项目(81260325);宁夏医科大学临床医学一流学科建设资助项目;2017年宁夏“研究生教育创新计划”学位点建设资助项目(YXW2017014)
语种:中文
中文关键词:结肠肿瘤;细胞增殖;肿瘤侵袭;成纤维细胞
外文关键词:Colonic neoplasms ; Cell proliferation ; Neoplasm invasiveness ; Fibroblasts
摘要:目的探讨成纤维细胞起源的CXCL12对结肠癌细胞CXCL8的影响及二者共同调控结肠癌增殖和转移的机制。方法应用Western blot技术检测5种结肠癌细胞(DLD-1、HT29、WiDr、CaCo-2、Col0320)、人脐静脉内皮细胞(HUVEC)中CXCL8和CXCL12的表达,应用ELISA技术检测CXCL8和CXCL12在结肠癌细胞和基质细胞中表达水平,应用细胞增殖和侵袭实验分别检测CXCL8和CXCL12在结肠癌细胞和HUVEC增殖和侵袭过程中的相互作用。结果CXCL12仅在成纤维细胞和DLD-1中高表达,CXCL8在所有结肠癌细胞、成纤维细胞和HUVEC中高表达;成纤维细胞来源的CXCL12能够显著增强CXCL8在CaCo-2、WiDr、HT-29和HUVEC中的表达(分别为2.54、2.07、1.87、2.79倍,均P〈0.01):CXCL8和CXCL12以浓度依赖性的方式促进HUVEC的增殖能力(P〈0.01)及HT-29和HUVEC的侵袭能力(P〈0.01)。结论成纤维细胞来源的CXCL12能够增强CXCL8在结肠癌细胞和HUVEC中的分泌,并且CXCL8和CXCL12均能促进结肠癌细胞的增殖和侵袭能力。
Objective To investigate the effect of CXCL12 on the secretion of CXCL8 from colon cancer cells and the mechanism of co-regulation of proliferation and metastasis of colon cancer. Methods The expression levels of CXCL8 and CXCL12 in 5 human colon cancer cell lines ( DLD-1, HT29, WiDr, CaCo-2, Colo320), fibroblasts, and human umbilical vein endothelial cells (HUVEC) were studied by Western blotting, respectively. ELISA, proliferation and invasion assay were used to explore the role of CXCL12 and CXCL8 for metastatic process of colon cancer and interaction between colon cancer cell and stromal cell in the microenvironment, respectively. Results The expression of CXCL8 was detected in all colon cancer cell lines, fibroblasts and HUVEC, while CXCL12 was expressed only in DLD-1 cell and fibroblast. The secretion level of CXCL8 in CaCo-2, WiDr, HT-29 and HUVEC (2. 54-fold vs. control, 2. 07- fold vs. control,1.87-fold vs. control, 2. 79-fold vs. control) was enhanced by CXCL12 that derived from fibroblasts(P 〈 0. 01 ). CXCL8 could significantly promote the proliferation, migration of HUVEC (P 〈 0. 01 ). CXCL8 and CXCL12 enhanced proliferation of HUVEC(P 〈0. 01 ) , invasion of HUVEC and HT -29 (P 〈 0. 01 )in a concentration-dependent manner. Conclusion Fibroblasts derived CXCL12 enhanced the CXCL8 secretion in colon cancer cells, and CXCL8 and CXCL12 can promote the proliferation and invasion of colon cancer cells.
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