Please enter verification code
Confirm
Effects of Apigenin on the Expressions of TGF-β1R II, NF-κB and VEGF Genes in Tumor Tissues of Mice with H29 Colon Cancer
American Journal of Clinical and Experimental Medicine
Volume 3, Issue 6, November 2015, Pages: 378-382
Received: Dec. 24, 2015; Published: Dec. 30, 2015
Views 3961      Downloads 119
Authors
Na Yi, College of Pharmacy, Inner Mongolia Medical University, Hohhot, China
Lengge Si, College of Mongolian Medicine, Inner Mongolia Medical University, Hohhot, China
Yuehong Wang, College of Mongolian Medicine, Inner Mongolia Medical University, Hohhot, China
Lidao Bao, College of Pharmacy, Inner Mongolia Medical University, Hohhot, China
Article Tools
Follow on us
Abstract
To observe the effects of Apigenin on the expressions of TGF-β1R II, NF-κB and VEGF genes in tumor tissues of mice with H29 colon cancer. Fifty ICR mice with H29 colon cancer were randomly divided into five groups: normal saline group, low-dose Apigenin group, middle-dose Apigenin group and high-dose Apigenin group and cyclophosphamide group. The mice were killed on the next day of administration discontinuance, and subcutaneous tumor tissues were collected. Quantitative fluorescence RT-PCR was used to detect the expression of TGF-β1R II, NF-κB and VEGF genes in tumor tissues of H29 colon cancer mice. Apigenin raised the expression level of TGF-β1R II in H29 colon cancer tissues, which showed the most obvious effect in the middle-dose group, with a significant difference compared with the normal saline group (P<0.01). The Apigenin group of each dose could significantly lower the NF-κB expression level in H29 colon solid tumors, showing significant differences compared with the normal saline group (P<0.01). The middle-dose and high-dose Apigenin groups could significantly reduce the level of VEGF expression in tumor tissues of ICR mice with H29 colon cancer, and the high-dose group had most obvious effect, and there were significant difference among the middle-dose group, high-dose group and the normal saline group (P<0.01). The mechanism of anti-tumor effect of Apigenin might be the reason that Apigenin can raise the expression level of TGF-β1R II by down-regulating the expression of NF–κB and VEGF in tumor tissues of tumor-bearing mice, thereby inhibiting tumor angiogenesis and tumor cell proliferation, so as to achieve the anti-tumor effect.
Keywords
Apigenin, H29 Colon Cancer, TGF-β1RII, NF-κB, VEGF
To cite this article
Na Yi, Lengge Si, Yuehong Wang, Lidao Bao, Effects of Apigenin on the Expressions of TGF-β1R II, NF-κB and VEGF Genes in Tumor Tissues of Mice with H29 Colon Cancer, American Journal of Clinical and Experimental Medicine. Vol. 3, No. 6, 2015, pp. 378-382. doi: 10.11648/j.ajcem.20150306.20
References
[1]
Park SW, Cho CS, Jun HO, et al. Anti-angiogenic effect of Apigenin on retinal neovascularization via blockade of reactive oxygen species production. Invest Ophthalmol Vis Sci, 2012, 19: 7718-7726.
[2]
Lim do Y, Cho HJ, Kim J, et al. Apigenin decreases IGF-II production and downregulates insulin-like growth factor-I receptor signaling in ht-29 human colon cancer cells. BMC Gastroenterol, 2012, 23: 9.
[3]
Pandurangan AK, Dharmalingam P, Ananda Sadagopan SK, et al. Effect of Apigenin on the levels of glycoproteins during azoxymethane-induced colon carcinogenesis in mice. Asian Pac J Cancer Prev, 2012, 13: 1569-1573.
[4]
Markaverich B, AlejandroM. Bioflavonoids, type II [H-3]estradiol binding sites and prostatic cancer cell proliferation. Int J Oncol, 1997, 11: 6.
[5]
Gates MA, Tworoger SS, Hecht JL, et al. A prospective study of dietary flavonoid intake and incidence of epithelial ovarian cancer. Int J Cancer, 2007, 121: 2225-2232.
[6]
Chen SS, Michael A, Butler-Manuel SA. Advances in the treatment of ovarian cancer: A potential role of antiinflammatory phytochemicals. Discov Med, 2012, 13: 7-17.
[7]
Lim do Y, Jeong Y, Tyner AL, et al. Induction of cell cycle arrest and apoptosis in ht-29 human colon cancer cells by the dietary compound Apigenin. Am J Physiol Gastrointest Liver Physiol, 2007, 292: G66-75.
[8]
Xie YY, Yuan D, Yang JY, et al. Cytotoxic activity of flavonoids from the flowers of chrysanthemum morifolium on human colon cancer colon205 cells. J Asian Nat Prod Res, 2009, 11: 771-778.
[9]
Keku TO, Vidal A, Oliver S, et al. Genetic variants in IGF-I, IGF-II, IGFBP-3, and adiponectin genes and colon cancer risk in african americans and whites. Cancer Causes Control, 2012, 23: 1127-1138.
[10]
Kyle AH, Baker JH, Minchinton AI. Targeting quiescent tumor cells via oxygen and igf-i supplementation. Cancer Res, 2012, 72: 801-809.
[11]
Li F, Cao Y, Townsend C M, Jr., et al. Tgf-beta signaling in colon cancer cells. World J Surg, 2005, 29: 306-311.
[12]
Markowitz S, Wang J, Myeroff L, et al. Inactivation of the type II TGF-beta receptor in colon cancer cells with microsatellite instability. Science, 1995, 268: 1336-1338.
[13]
Becker C, Fantini M C, Schramm C, et al. TGF-beta suppresses tumor progression in colon cancer by inhibition of il-6 trans-signaling. Immunity, 2004, 21: 491-501.
[14]
Bellam N, Pasche B. TGF-beta signaling alterations and colon cancer. Cancer Treat Res, 2010, 155: 85-103.
[15]
Dornhoff H, Becker C, Wirtz S, et al. A variant of smurf2 protects mice against colitis-associated colon cancer by inducing transforming growth factor beta signaling. Gastroenterology, 2012, 142: 1183-1194 e4.
[16]
Nakagawa Y, Akao Y. Fhit protein inhibits cell growth by attenuating the signaling mediated by nuclear factor-kappab in colon cancer cell lines. Exp Cell Res, 2006, 312: 2433-2442.
[17]
Okayama T, Kokura S, Ishikawa T, et al. Antitumor effect of pretreatment for colon cancer cells with hyperthermia plus geranylgeranylacetone in experimental metastasis models and a subcutaneous tumor model of colon cancer in mice. Int J Hyperthermia, 2009, 25: 141-149.
[18]
Seufert B L, Poole E M, Whitton J, et al. IkappabκBeta and nfkappab1, nsaid use and risk of colorectal cancer in the colon cancer family registry. Carcinogenesis, 2013, 34: 79-85.
[19]
Yun J W, Lee W S, Kim M J, et al. Characterization of a profile of the anthocyanins isolated from vitis coignetiae pulliat and their anti-invasive activity on ht-29 human colon cancer cells. Food Chem Toxicol, 2010, 48: 903-909.
[20]
Yonezawa M, Wada K, Tatsuguchi A, et al. Heregulin-induced vegf expression via the erbb3 signaling pathway in colon cancer. Digestion, 2009, 80: 215-225.
[21]
Zhang Y, Liu X, Zhang J, et al. The expression and clinical significance of pi3k, pakt and vegf in colon cancer. Oncol Lett, 2012, 4: 763-766.
[22]
Adachi S, Yasuda I, Nakashima M, et al. Rho-kinase inhibitor upregulates migration by altering focal adhesion formation via the akt pathway in colon cancer cells. Eur J Pharmacol, 2011, 650: 145-150.
[23]
Akagi Y, Liu W, Xie K, et al. Regulation of vascular endothelial growth factor expression in human colon cancer by interleukin-1beta. Br J Cancer, 1999, 80: 1506-1511.
[24]
Bunger S, Haug U, Kelly M, et al. A novel multiplex-protein array for serum diagnostics of colon cancer: A case-control study. BMC Cancer, 2012, 12: 393.
[25]
Cacev T, Loncar B, Seiwerth S, et al. Vascular endothelial growth factor polymorphisms -1154 g/a and -460 c/t are not associated with vegf mrna expression and susceptibility to sporadic colon cancer. DNA Cell Biol, 2008, 27: 569-574.
[26]
Cascinu S, Graziano F, Catalano V, et al. Differences of vascular endothelial growth factor (VEGF) expression between liver and abdominal metastases from colon cancer. Implications for the treatment with vegf inhibitors. Clin Exp Metastasis, 2000, 18: 651-655.
ADDRESS
Science Publishing Group
1 Rockefeller Plaza,
10th and 11th Floors,
New York, NY 10020
U.S.A.
Tel: (001)347-983-5186