Effects of Advanced Glycosylation End Products on Proliferation of Human Colon Carcinoma Cell Line SW-480 and Its Mechanism_West China Medical Journal

Authors：

ZHOU Xiaozhi ^1,2 ,  XUE Yaoming ¹ , GUAN Meiping ¹ , ZHU Bo ¹

1. Department of Endocrinology and Metabolism, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, P. R. China; 2. Department of Endocrinology, Central Hospital of Ji′an, Ji′an, Jiangxi 343000, P.R.China;

Corresponding author：

XUE Yaoming, Email: zxz20020013@163.com

Keywords：

晚期糖基化终产物; SW-480细胞; 细胞周期; CyclinD1; 端粒酶活性

Video：

Export PDF Favorites Scan Get Citation

Abstract Full text Figures/Tables Video References Cited by

【摘要】　目的　观察晚期糖基化终产物（advanced glycosylation end prodrcts，AGE）对人结肠癌细胞株SW-480增殖的影响，并探讨其可能机制。　方法　不同浓度AGE干预SW-480细胞，噻唑蓝（MTT）法比较各组细胞活力，流式细胞术观察AGE对SW-480细胞周期的影响，蛋白质印迹法观察AGE对SW-480细胞CyclinD1表达的影响，端粒重复序列扩增法（telomeric repeat amplification protocol，TRAP）银染法观察AGE对SW-480细胞端粒酶活性的影响。MTT测细胞活力的检测设置空白对照组、100 μg/mL小牛血清白蛋白（bovine serum albumin，BSA）组及50、100、500 μg/mL AGE组，其余检测只设置100 μg/mL BSA组和100 μg/mL AGE组。　结果　 MTT结果示AGE促进SW-480细胞的增殖，且呈浓度依赖性。100 μg/mL BSA组与100 μg/mL AGE组72 h后的细胞G0/G1期所占百分比分别为56.02%±0.58%、51.93%±1.01%，差异有统计学意义（P lt;0.05）。蛋白质印迹法示100 μg/mL AGE组72 h后CyclinD1的表达较100 μg/mL BSA组增加，差异有统计学意义（P lt;0.05）。TRAP银染法检测示100 μg/mL AGE干预SW-480细胞72 h后可以增加端粒酶活性（P lt;0.05）。　结论　 AGE可促进人结肠癌细胞SW-480生长，呈剂量依赖性。其作用机制可能与AGE上调CyclinD1的表达加速G1/S期转换及增加端粒酶活性有关。
【Abstract】　Objective　 To observe the effects of advanced glycosylation end products (AGE) on proliferation of SW-480 cells and study the possible mechanism.　Methods　 Various concentrations of AGE were designed to have impact on SW-480 cells. Proliferation of SW-480 cells was assessed by thiazolyl blue tetrazolium bromide (MTT) assay; The impact of AGE on the cell cycle of SW-480 cells was analyzed by flow cytometry (FCM); the influence of AGE on expression of CyclinD1 was checked by Western blotting; and the impact of AGE on telomerase activity was examined by telomeric repeat amplification proctol (TRAP) sliver staining. For the MTT assay, blank control group, 100 μg/mL bovine serum albumin (BSA) group, 50, 100 and 500 μg/mL AGE groups were designed, while for other examinations, there were only 100 μg/mL BSA group and 100 μg/mL AGE group.　Results　 MTT result showed that AGE increased the proliferation of SW-480 cells in a dose-dependent mode. The proportion of the cells at G0/G1 stage of the 100 μg/mL BSA group and the 100 μg/mL AGE experimental group were (56.02±0.58)% and (51.93±1.01)% respectively after 72 hours, with a significant difference (P lt;0.05); western blotting showed that the expression of CyclinD1 in the 100 μg/mL AGE group was significantly higher than that in the 100 μg/mL BSA group after 72 hours; TRAP silver staining demonstrated that telomerase activity increased significantly after treated with 100 μg/mL AGE for 72 hours.　Conclusions　 AGE can promote the growth of SW-480 cells in a dose-dependent mode. Its mechanism is mainly by up-regulating the expression of CyclinD1 to shorten G0/G1 and increasing the telomerase activity significantly.

Citation： ZHOU Xiaozhi,XUE Yaoming,GUAN Meiping,ZHU Bo. Effects of Advanced Glycosylation End Products on Proliferation of Human Colon Carcinoma Cell Line SW-480 and Its Mechanism. West China Medical Journal, 2011, 26(6): 837-841. doi: Copy

1.	Stattin P, Bjor O, Ferrari P, et al. Prospective study of hyperglycemia and cancer risk[J]. Diabetes Care, 2007, 30(3): 561-567.
2.	Inoue M, Iwasaki M, Otani T, et al. Diabetes mellitus and the risk of cancer: results from a large-scale population-based cohort study in Japan[J]. Arch Intern Med, 2006, 166(17): 1871-1877.
3.	Vigneri P, Frasca F,Sciacca L, et al. Diabetes and cancer[J].Encocrine-Related Cancer, 2009,16(4): 1103-1123.
4.	Edward F, Tierney MPH, Linda S. Population-based estimates of mortality associated with diabetes: use of a death certificate check box in North Dakota[J]. Am J Public Health, 2001, 91(1): 84-92.
5.	Abe R, Shimizu T, Sugawara H, et al. Regulation of human melanoma growth and metastasis by AGE-AGE receptor interactions[J]. J Invest Dermatol, 2004, 122(2): 461-467.
6.	Abe R, Yamagishi S. AGE-RAGE system and carcinogenesis[J]. Curr Pharm Des, 2008, 14(10): 940-945.
7.	王爱萍, 胡水清, 汤哲, 等. 糖尿病与结直肠癌患病危险关系的调查分析[J]. 世界华人消化杂志, 2007, 15(1): 88-91.
8.	Jullumstro E, Kollind M, Lydersen S, et al. Diabetes mellitus and outcomes of colorectal cancer[J]. Acta Oncol, 2009, 48(3): 361-367.
9.	Berster JM, Goke B. Type 2 diabetes mellitus as risk factor for colorectal cancer[J]. Arch Physiol Biochem, 2008, 114(1): 84-98.
10.	Larsson SC, Orsini N, Wolk A. Diabetes mellitus and risk of colorectal cancer: a meta-analysis[J]. J Natl Cancer Inst, 2005, 97(22): 1679-1687.
11.	Yamagishi S, Nakamura K, Inoue H, et al. Possible participation of advanced glycation end products in the pathogenesis of colorectal cancer in diabetic patients[J]. Med Hypotheses, 2005, 64(6): 1208-1210.
12.	王瑞良, 苏青, 等.RAGE及其配体的临床意义研究进展[J]. 国际内分泌代谢杂志, 2006, 26(3): 160-162.
13.	Miki S, Kasayama S, Miki Y, et al. Expression of receptors for advanced glycosylation end products on renal cell carcinoma cells in vitro[J]. Biochem Biophys Res Commun, 1993, 196(2): 984-989.
14.	Yamamoto Y, Yamagishi S, Hsu CC, et al. Advanced glycation end products-receptor interactions stimulate the growth of human pancreatic cancer cells through the induction of platelet-derived growth factor-B[J]. Biochem Biophys Res Commun, 1996, 222(3): 700-705.
15.	Fuentes MK, Nigavekar SS, Arumugam T, et al. RAGE activation by S100P in colon cancer stimulates growth, migration and cell signaling pathway[J]. Dis Colon Rectum 2007, 50(8): 1230-1240.
16.	Kuniyasu H, Chihara Y, Takahashi T. Co-expression of receptor for advanced glycation end products and the ligand amphoterin associates closely with metastasis of colorectal cancer [J]. Oncol Rep, 2003, 10(2): 445-448.
17.	Ishiguro H, Nakaigawa N, Miyoshi Y, et al. Receptor for advanced glycation end products (RAGE) and its ligand, amphoterin are overexpressed and associated with prostate cancer development [J]. Prostate, 2005, 64(1): 92-100.
18.	Guh JY, Huang JS, Chen HC, et al. Advanced glycation end product-induced proliferation in NRK-49F cells is dependent on the JAK2/STAT5 pathway and cyclin D1[J]. Am J Kidney Dis, 2001, 38(5): 1096-1104.
19.	Kim JY, Park HK, Yoon JS, et al. Advanced glycation end product (AGE)-induced proliferation of HEL cells via receptor for AGE-related signal pathways[J]. Int J Oncol, 2008, 33(3): 493-501.
20.	Zill H, Gunther R, Erbersdobler HF, et al. RAGE expression and AGE-induced MAP kinase activation in Caco-2 cells[J]. Biochem Biophys Res Commun, 2001, 288(5): 1108-1111.
21.	Kuniyasu H, Chihara Y, Kondo H.Differential effects between amphoterin and advanced glycation end products on colon cancer cells[J]. Int J Cancer, 2003, 104(6): 722-727.
22.	Boldrini L, Faviana P, Gisfredi S, et al. Evaluation of telomerase in the development and progression of colon cancer [J]. Int J Mol Med, 2002, 10(5): 589-592.
23.	Holt SE, Wright WE, Shay JW. Multiple pathways for the regulation of telomerase activity [J]. Eur J Cancer, 1997, 33(5): 761-766.

1. 　Stattin P, Bjor O, Ferrari P, et al. Prospective study of hyperglycemia and cancer risk[J]. Diabetes Care, 2007, 30(3): 561-567.
2. 　Inoue M, Iwasaki M, Otani T, et al. Diabetes mellitus and the risk of cancer: results from a large-scale population-based cohort study in Japan[J]. Arch Intern Med, 2006, 166(17): 1871-1877.
3. 　Vigneri P, Frasca F,Sciacca L, et al. Diabetes and cancer[J].Encocrine-Related Cancer, 2009,16(4): 1103-1123.
4. 　Edward F, Tierney MPH, Linda S. Population-based estimates of mortality associated with diabetes: use of a death certificate check box in North Dakota[J]. Am J Public Health, 2001, 91(1): 84-92.
5. 　Abe R, Shimizu T, Sugawara H, et al. Regulation of human melanoma growth and metastasis by AGE-AGE receptor interactions[J]. J Invest Dermatol, 2004, 122(2): 461-467.
6. 　Abe R, Yamagishi S. AGE-RAGE system and carcinogenesis[J]. Curr Pharm Des, 2008, 14(10): 940-945.
7. 　王爱萍, 胡水清, 汤哲, 等. 糖尿病与结直肠癌患病危险关系的调查分析[J]. 世界华人消化杂志, 2007, 15(1): 88-91.
8. 　Jullumstro E, Kollind M, Lydersen S, et al. Diabetes mellitus and outcomes of colorectal cancer[J]. Acta Oncol, 2009, 48(3): 361-367.
9. 　Berster JM, Goke B. Type 2 diabetes mellitus as risk factor for colorectal cancer[J]. Arch Physiol Biochem, 2008, 114(1): 84-98.
10. 　Larsson SC, Orsini N, Wolk A. Diabetes mellitus and risk of colorectal cancer: a meta-analysis[J]. J Natl Cancer Inst, 2005, 97(22): 1679-1687.
11. 　Yamagishi S, Nakamura K, Inoue H, et al. Possible participation of advanced glycation end products in the pathogenesis of colorectal cancer in diabetic patients[J]. Med Hypotheses, 2005, 64(6): 1208-1210.
12. 　王瑞良, 苏青, 等.RAGE及其配体的临床意义研究进展[J]. 国际内分泌代谢杂志, 2006, 26(3): 160-162.
13. 　Miki S, Kasayama S, Miki Y, et al. Expression of receptors for advanced glycosylation end products on renal cell carcinoma cells in vitro[J]. Biochem Biophys Res Commun, 1993, 196(2): 984-989.
14. 　Yamamoto Y, Yamagishi S, Hsu CC, et al. Advanced glycation end products-receptor interactions stimulate the growth of human pancreatic cancer cells through the induction of platelet-derived growth factor-B[J]. Biochem Biophys Res Commun, 1996, 222(3): 700-705.
15. 　Fuentes MK, Nigavekar SS, Arumugam T, et al. RAGE activation by S100P in colon cancer stimulates growth, migration and cell signaling pathway[J]. Dis Colon Rectum 2007, 50(8): 1230-1240.
16. 　Kuniyasu H, Chihara Y, Takahashi T. Co-expression of receptor for advanced glycation end products and the ligand amphoterin associates closely with metastasis of colorectal cancer [J]. Oncol Rep, 2003, 10(2): 445-448.
17. 　Ishiguro H, Nakaigawa N, Miyoshi Y, et al. Receptor for advanced glycation end products (RAGE) and its ligand, amphoterin are overexpressed and associated with prostate cancer development [J]. Prostate, 2005, 64(1): 92-100.
18. 　Guh JY, Huang JS, Chen HC, et al. Advanced glycation end product-induced proliferation in NRK-49F cells is dependent on the JAK2/STAT5 pathway and cyclin D1[J]. Am J Kidney Dis, 2001, 38(5): 1096-1104.
19. 　Kim JY, Park HK, Yoon JS, et al. Advanced glycation end product (AGE)-induced proliferation of HEL cells via receptor for AGE-related signal pathways[J]. Int J Oncol, 2008, 33(3): 493-501.
20. 　Zill H, Gunther R, Erbersdobler HF, et al. RAGE expression and AGE-induced MAP kinase activation in Caco-2 cells[J]. Biochem Biophys Res Commun, 2001, 288(5): 1108-1111.
21. 　Kuniyasu H, Chihara Y, Kondo H.Differential effects between amphoterin and advanced glycation end products on colon cancer cells[J]. Int J Cancer, 2003, 104(6): 722-727.
22. 　Boldrini L, Faviana P, Gisfredi S, et al. Evaluation of telomerase in the development and progression of colon cancer [J]. Int J Mol Med, 2002, 10(5): 589-592.
23. 　Holt SE, Wright WE, Shay JW. Multiple pathways for the regulation of telomerase activity [J]. Eur J Cancer, 1997, 33(5): 761-766.

West China Medical Journal

Effects of Advanced Glycosylation End Products on Proliferation of Human Colon Carcinoma Cell Line SW-480 and Its Mechanism

Abstract Full text Figures/Tables Video References Cited by

Format

Content