实用肿瘤学杂志
實用腫瘤學雜誌
실용종류학잡지
JOURNAL OF PRACTICAL ONCOLOGY
2014年
4期
305-309
,共5页
肿瘤分子靶向治疗%半乳糖凝集素3%二羟甲基丁酸%对苯二甲酸%化学致癌
腫瘤分子靶嚮治療%半乳糖凝集素3%二羥甲基丁痠%對苯二甲痠%化學緻癌
종류분자파향치료%반유당응집소3%이간갑기정산%대분이갑산%화학치암
Tumor molecular targeted therapy%Galectin-3%Dimethyl benzanthracene%12-o-tetrade-canoylphorbol-13-acetate%Chemical carcinogenesis
目的:观察半乳糖凝集素3(Gal3)基因敲除对小鼠皮肤肿瘤生长产生的影响,探讨Gal3基因敲除抑制DMBA+TPA诱导小鼠皮肤肿瘤生长的机制。方法采用DMBA+TPA多步骤诱导小鼠皮肤癌模型方法建立皮肤癌发生模型。以同龄野生型小鼠为对照组观察Gal3基因敲除对小鼠肿瘤生长产生的影响,通过采集分离原位癌细胞进行体外软琼脂克隆培养,观察克隆形成情况。使用流式细胞仪对原位癌细胞进行side population定量解析,分析肿瘤干细胞在肿瘤细胞中比率。结果 Gal3基因敲除小鼠组(实验组)肿瘤出现时间与野生型小鼠组(对照组)相比显著延迟,肿瘤发生率及平均每只小鼠肿瘤个数对照组与实验组相比较有明显差异(P<0.01)。采集分离对照组与实验组原位肿瘤细胞进行体外软琼脂克隆培养,克隆形成率对照组明显高于实验组(P<0.01)。采集分离对照组、实验组原位肿瘤细胞,使用流式细胞仪对原位肿瘤细胞side population定量解析,对照组与实验组比较有统计学差异( P<0.01)。结论 Gal3基因敲除减少皮肤肿瘤干细胞数量并抑制肿瘤细胞增殖,减少化学致癌发生,抑制小鼠皮肤肿瘤生长。提示Gal3基因有可能成为皮肤癌化学治疗的新靶点。
目的:觀察半乳糖凝集素3(Gal3)基因敲除對小鼠皮膚腫瘤生長產生的影響,探討Gal3基因敲除抑製DMBA+TPA誘導小鼠皮膚腫瘤生長的機製。方法採用DMBA+TPA多步驟誘導小鼠皮膚癌模型方法建立皮膚癌髮生模型。以同齡野生型小鼠為對照組觀察Gal3基因敲除對小鼠腫瘤生長產生的影響,通過採集分離原位癌細胞進行體外軟瓊脂剋隆培養,觀察剋隆形成情況。使用流式細胞儀對原位癌細胞進行side population定量解析,分析腫瘤榦細胞在腫瘤細胞中比率。結果 Gal3基因敲除小鼠組(實驗組)腫瘤齣現時間與野生型小鼠組(對照組)相比顯著延遲,腫瘤髮生率及平均每隻小鼠腫瘤箇數對照組與實驗組相比較有明顯差異(P<0.01)。採集分離對照組與實驗組原位腫瘤細胞進行體外軟瓊脂剋隆培養,剋隆形成率對照組明顯高于實驗組(P<0.01)。採集分離對照組、實驗組原位腫瘤細胞,使用流式細胞儀對原位腫瘤細胞side population定量解析,對照組與實驗組比較有統計學差異( P<0.01)。結論 Gal3基因敲除減少皮膚腫瘤榦細胞數量併抑製腫瘤細胞增殖,減少化學緻癌髮生,抑製小鼠皮膚腫瘤生長。提示Gal3基因有可能成為皮膚癌化學治療的新靶點。
목적:관찰반유당응집소3(Gal3)기인고제대소서피부종류생장산생적영향,탐토Gal3기인고제억제DMBA+TPA유도소서피부종류생장적궤제。방법채용DMBA+TPA다보취유도소서피부암모형방법건립피부암발생모형。이동령야생형소서위대조조관찰Gal3기인고제대소서종류생장산생적영향,통과채집분리원위암세포진행체외연경지극륭배양,관찰극륭형성정황。사용류식세포의대원위암세포진행side population정량해석,분석종류간세포재종류세포중비솔。결과 Gal3기인고제소서조(실험조)종류출현시간여야생형소서조(대조조)상비현저연지,종류발생솔급평균매지소서종류개수대조조여실험조상비교유명현차이(P<0.01)。채집분리대조조여실험조원위종류세포진행체외연경지극륭배양,극륭형성솔대조조명현고우실험조(P<0.01)。채집분리대조조、실험조원위종류세포,사용류식세포의대원위종류세포side population정량해석,대조조여실험조비교유통계학차이( P<0.01)。결론 Gal3기인고제감소피부종류간세포수량병억제종류세포증식,감소화학치암발생,억제소서피부종류생장。제시Gal3기인유가능성위피부암화학치료적신파점。
Objective To observe the effect of Galectin -3 gene knock out to the mouse skin tumor growth and discuss the mechanism of inhibition of the mouse cutaneous tumor induced by 12 -o -tetrade-canoylphorbol-13-acetate which caused by Galectin -3 knock out.Methods The DMBA +TPA multi-step induced skin tumor in mice model were used to establish the skin cancer model .The control group was the same age wild type mice .We observed the inhibition of the mouse tumor growth by Galectin -3 knock out .In situ tumor cells were collected and cultured on soft agar for colony formation assay .The side population of the situ cancer cells was analyzed quantitatively by flow cytometry .Results 1.Compared with wild type mice group(group A), Galectin-3 knock out mice group ( group B) displayed a significant delay of the appearance of tumor .The tumor incidence and the average number of tumor per mice between group A and group B had obvious difference ( P<0.01).2.In vitro,data of soft agar colony formation assay showed that colony formation rate in group A are signif -icantly higher than group B(P<0.01).3.The collection and separation of A and B group in situ tumor cells ,u-sing flow cytometry instrument for in situ tumor cell side population quantitative analysis ,group A compared with group B had obvious difference(P<0.01).Conclusion The knock out of the Galectin -3 gene reduces the skin cancer stem cells ,inhibits tumor cell proliferation ,depresses chemical carcinogenesis of mice skin .Galectin-3 gene may become the new target for skin cancer chemotherapy .