目的:检测膀胱癌细胞中SPOCK1(sparc/osteonectin,cwcv and kazal-like domains proteoglycan 1)基因的表达情况,并进一步研究下调SPOCK1基因表达对膀胱癌细胞增殖、迁移和侵袭的影响。方法 :采用实时荧光定量PCR和蛋白质印迹法检测人...目的:检测膀胱癌细胞中SPOCK1(sparc/osteonectin,cwcv and kazal-like domains proteoglycan 1)基因的表达情况,并进一步研究下调SPOCK1基因表达对膀胱癌细胞增殖、迁移和侵袭的影响。方法 :采用实时荧光定量PCR和蛋白质印迹法检测人输尿管上皮永生化细胞SV-HUC-1以及膀胱癌细胞株5637和T24中SPOCK1基因的表达情况。构建特异性针对SPOCK1基因的si RNA片段,并将其通过脂质体介导转染至膀胱癌5637细胞;同时设立未转染的空白对照组和转染无义序列的阴性对照组。采用实时荧光定量PCR法和蛋白质印迹法检测各组细胞中SPOCK1 m RNA和蛋白的表达差异。然后采用CCK-8法、划痕愈合实验和Transwell小室法分别检测SPOCK1基因表达下调后膀胱癌细胞增殖、迁移和侵袭能力的变化情况。结果 :膀胱癌细胞中SPOCK1基因表达水平高于输尿管上皮永生化细胞,尤以膀胱癌5637细胞中的表达水平最高(P值均<0.05)。SPOCK1 si RNA转染后,膀胱癌5637细胞中SPOCK1基因的表达明显下调(P<0.05),而膀胱癌细胞的增殖、迁移和侵袭能力均被明显抑制(P值均<0.05)。结论:膀胱癌细胞中SPOCK1基因存在过表达现象。下调SPOCK1基因表达可以降低膀胱癌5637细胞的增殖、迁移和侵袭能力。展开更多
supported by the Earmarked Fund for the Modern Agroindustry Technology Research System, China （CARS-41）;the National High Technology Research and Development Program of China （2011AA100301）
Objective: To investigate the changes of oncogene Dickkopf 2 (DKK2) and sparc/osteonectin, cwcv and kazal-like domains proteoglycan 1 (SPOCK1) expression in bladder cancer lesions and their correlation with cancer cel...Objective: To investigate the changes of oncogene Dickkopf 2 (DKK2) and sparc/osteonectin, cwcv and kazal-like domains proteoglycan 1 (SPOCK1) expression in bladder cancer lesions and their correlation with cancer cell proliferation and invasion. Methods: The bladder cancer lesions and paracancerous lesions surgically removed in our hospital between March 2016 and March 2018 were collected, and kits were used to measure the mRNA expression levels of DKK2, SPOCK1, proliferation genes and invasion genes. Results: DKK2, hyperplasia suppressor gene (HSG), p16, cell adhesion molecule-1 (CADM1), tissue inhibitor of matrix metalloproteinase 2 (TIMP2) and TIMP4 mRNA expression in bladder cancer lesions were significantly lower than those in paracancerous lesions while SPOCK1, β-catenin, CyclinD1, c-myc, Vimentin and matrix metalloproteinase 2 (MMP2) mRNA expression were significantly higher than those in paracancerous lesions;DKK2 was negatively correlated with β-catenin, CyclinD1, c-myc, Vimentin and MMP2, and positively correlated with HSG, p16, CADM1, TIMP2 and TIMP4;SPOCK1 was positively correlated with β-catenin, CyclinD1, c-myc, Vimentin and MMP2, and negatively correlated with HSG, p16, CADM1, TIMP2 and TIMP4. Conclusion: The low expression of oncogene DKK2 and the high expression of SPOCK1 in bladder cancer lesions are related to the changes of proliferation and invasion genes and may be involved in the growth of lesions.展开更多
文摘目的:检测膀胱癌细胞中SPOCK1(sparc/osteonectin,cwcv and kazal-like domains proteoglycan 1)基因的表达情况,并进一步研究下调SPOCK1基因表达对膀胱癌细胞增殖、迁移和侵袭的影响。方法 :采用实时荧光定量PCR和蛋白质印迹法检测人输尿管上皮永生化细胞SV-HUC-1以及膀胱癌细胞株5637和T24中SPOCK1基因的表达情况。构建特异性针对SPOCK1基因的si RNA片段,并将其通过脂质体介导转染至膀胱癌5637细胞;同时设立未转染的空白对照组和转染无义序列的阴性对照组。采用实时荧光定量PCR法和蛋白质印迹法检测各组细胞中SPOCK1 m RNA和蛋白的表达差异。然后采用CCK-8法、划痕愈合实验和Transwell小室法分别检测SPOCK1基因表达下调后膀胱癌细胞增殖、迁移和侵袭能力的变化情况。结果 :膀胱癌细胞中SPOCK1基因表达水平高于输尿管上皮永生化细胞,尤以膀胱癌5637细胞中的表达水平最高(P值均<0.05)。SPOCK1 si RNA转染后,膀胱癌5637细胞中SPOCK1基因的表达明显下调(P<0.05),而膀胱癌细胞的增殖、迁移和侵袭能力均被明显抑制(P值均<0.05)。结论:膀胱癌细胞中SPOCK1基因存在过表达现象。下调SPOCK1基因表达可以降低膀胱癌5637细胞的增殖、迁移和侵袭能力。
基金supported by the Earmarked Fund for the Modern Agroindustry Technology Research System, China (CARS-41)the National High Technology Research and Development Program of China (2011AA100301)
文摘supported by the Earmarked Fund for the Modern Agroindustry Technology Research System, China （CARS-41）;the National High Technology Research and Development Program of China （2011AA100301）
文摘Objective: To investigate the changes of oncogene Dickkopf 2 (DKK2) and sparc/osteonectin, cwcv and kazal-like domains proteoglycan 1 (SPOCK1) expression in bladder cancer lesions and their correlation with cancer cell proliferation and invasion. Methods: The bladder cancer lesions and paracancerous lesions surgically removed in our hospital between March 2016 and March 2018 were collected, and kits were used to measure the mRNA expression levels of DKK2, SPOCK1, proliferation genes and invasion genes. Results: DKK2, hyperplasia suppressor gene (HSG), p16, cell adhesion molecule-1 (CADM1), tissue inhibitor of matrix metalloproteinase 2 (TIMP2) and TIMP4 mRNA expression in bladder cancer lesions were significantly lower than those in paracancerous lesions while SPOCK1, β-catenin, CyclinD1, c-myc, Vimentin and matrix metalloproteinase 2 (MMP2) mRNA expression were significantly higher than those in paracancerous lesions;DKK2 was negatively correlated with β-catenin, CyclinD1, c-myc, Vimentin and MMP2, and positively correlated with HSG, p16, CADM1, TIMP2 and TIMP4;SPOCK1 was positively correlated with β-catenin, CyclinD1, c-myc, Vimentin and MMP2, and negatively correlated with HSG, p16, CADM1, TIMP2 and TIMP4. Conclusion: The low expression of oncogene DKK2 and the high expression of SPOCK1 in bladder cancer lesions are related to the changes of proliferation and invasion genes and may be involved in the growth of lesions.
