摘要
目的探讨趋化因子联接因子1(CXCL1)促进卵巢癌细胞增殖与解整合素—金属蛋白酶(ADAM)10-表皮生长因子受体(EGFR)通路的关系。方法 SPF级免疫缺陷型SCID雌性小鼠9只,随机分为三组:卵巢上皮癌(SKOV3)细胞组采用体外培养的卵巢癌细胞系SKOV3,GFP-SKOV3细胞组采用体外培养的卵巢癌细胞系GFP-SKOV3,CXCL1过表达(CXCL1-GFP-SKOV3)细胞组过表达CXCL1基因的CXCL1-GFP-SKOV3建立裸鼠皮下成瘤模型,30 d后取皮下瘤组织,采用脊髓离断法处死裸鼠,无菌剥离瘤体,比较各组肿瘤生长重量;采用实时荧光定量PCR法检测ADAM10、肝素结合表皮生长因子样生长因子(HBEGF)、EGFR及CXCL1基因表达。结果 CXCL1-GFP-SKOV3组产生的移植瘤重量显著高于GFP-SKOV3细胞组和SKOV3细胞组(P均<0.01);ADAM10、HBEGF、EGFR及CXCL1四个基因在CXCL1-GFP-SKOV3细胞的表达均显著高于GFP-SKOV3细胞组和SKOV3细胞组(P均<0.01)。结论趋化因子CXCL1可能通过激活ADAM10-EGFR途径进而促进卵巢癌细胞的增殖。
Objective To investigate the relationship between CXCL1 overexpression in promoting the proliferation of ovarian cancer and a disintegrin and metalloproteinase-lO-epidermal growth factor receptor (ADAM10-EGFR) pathway. Methods A total of 9 SCID female mice with SPF immunodeficiency were randomly divided into three groups: SKOV3 group ( cultured in vitro in ovarian cancer cell lines SKOV3 ), GFP-SKOV3 group ( cultured in vitro in ovarian cancer cell lines GFP-SKOV3 ) and CXCLI-GFP-SKOV3 group (established nude mice subcutaneous tumor model with overexpression of CXCL1 gene). 30d later, the subcutaneous tumor tissues were extracted, the nude mice were killed by spinal cord tran- section, and the tumors were removed under the sterile condition, tumor growth weight in different groups was compared. The expressions of ADAM10, heparin binding epidermal growth factors (HBEGF), EGFR and CXCL1 gene were detected by real-time fluorescent quantitative PCR. Results The weight of xenograft tumor in CXCL1-GFP-SKOV3 group was sig- nificantly higher than those in GFP-SKOV3 group and SKOV3 group ( all P 〈 0. O1 ). The expressions of ADAM10, HBEGF, EGFR and CXCL1 were significantly higher in CXCL1-GFP-SKOV3 group than those in GFP-SKOV3 group and SKOV3 group (all P 〈 O. 01 ). Conclusion The chemokine CXCLI may activate the ADAMI0-EGFR pathway, thus can- tribute to the proliferation of ovarian cancer cells.
出处
《山东医药》
CAS
2013年第19期25-27,共3页
Shandong Medical Journal
基金
广西2011年研究生教育创新计划资助项目(2011105981-002M183)