Document Type : Original Article


1 Department of Biology, Islamic Azad University of Parand Branch, Parand, Iran

2 Department of Biotechnology, Islamic Azad University of Parand Branch, Parand, Iran.

3 Department of genetics,faculty of science,islamic azad university of central tehran branch,Tehran, Iran



Introduction Colorectal cancer is the second and third most common cancer in women and men respectively. Early diagnosis of illness will reduce pain and costs for patients. In this study, the expression of fgf19 gene in different individuals with colorectal cancer, and also the relationship between the expression of this gene and the degree and stage of cancer cells, will be evaluated.
Methods A total of 60 samples were collected by a surgeon from cancerous tissue and healthy marginal tissue of patients with colorectal cancer. Extraction of RNA was accomplished by a Trizol solution. In the next step, cDNA molecule was synthesized using reverse transcriptase enzyme (RT), and gene-specific primers were designed and synthesized. Then the expression of FGF19 gene was evaluated by Real-time PCR technique. Finally, the data obtained from cancerous tissue and healthy marginal tissue were analyzed by spss software.
Result The expression of fgf19 in tumor tissue and healthy marginal tissue was measured quantitatively, which increased by 56.7 percent.
Conclusion The results of this study indicate that fgf19 as a molecular biomarker plays a significant role in the progression of cancer, and therefore can be considered as a factor in the screening, early detection, prognosis and predictor of the tumor.


Main Subjects

Bernard, PS, Wittwer, CT. (2002). Real-Time PCR technology for cancer diagnostics. Clin Chem, 48(8):1178-1185.
Capelle, LG, Van Grieken, NC, Lingsma, HF, Steyerberg, EW, Klokman, WJ, Bruno, MJ, Vasen, HF, Kuipers, EJ. (2010).  Risk and epidemiological time trends of gastric cancer in Lynch syndrome carriers in the Netherlands. Gastroenterology. 138:487–92. [PubMed: 19900449].
Coskun, T, Bina, HA, Schneider, MA, Dunbar, JD, Hu, CC, Chen, Y, Moller, DE, Kharitonenkov, A. (2008). Fibroblast growth factor 21 corrects obesity in mice. Endocrinology. 149:6018–6027.
Fukumoto, S (2008). Actions and mode of actions of FGF19 subfamily members. Endocr J, 55:23–31.
Fu, L, John, LM, Adams, SH, Yu, XX, Tomlinson, E, Renz, M, Williams, PM, Soriano, R, Corpuz, R, Moffat, B, Vandlen, R, Simmons, L, Foster, J, Stephan, JP, Tsai, SP, Stewart, TA. (2004). Fibroblast growth factor 19 increases metabolic rate and reverses dietary and leptindeficient diabetes. Endocrinology 145: 2594–2603.
Globocan. 2012. at
Inagaki, T, Dutchak, P, Zhao, G, Ding, X, Gautron, L, Parameswara, V, Li, Y, Goetz, R, Mohammadi, M, Esser, V, Elmquist, JK, Gerard, RD, Burgess, SC, Hammer, RE, Mangelsdorf, DJ, Kliewer, SA. (2007). Endocrine Regulation of the Fasting Response by PPARalpha-Mediated Induction of Fibroblast Growth Factor 21. Cell Metab, 5:415–425.
Jones, S. (2008) Mini-review: endocrine actions of fibroblast growth factor 19. Mol Pharm 5:42–48.
Kharitonenkov, A, Larsen, P. (2011) FGF21 reloaded: challenges of a rapidly growing field. Trends Endocrinol Metab. 22:81–86.
Kuipers, EJ, Rösch, T, Bretthauer, M. (2013). Colorectal cancer screening--optimizing current strategies and new directions. Nat Rev Clin Oncol. 10:130–42. Review of current state of art of colorectal cancer screening. [PubMed: 23381005].
Li, X, Ge, H, Weiszmann, J, Hecht, R, Li, YS, Véniant ,MM, Xu, J, Wu, X, Lindberg, R, Li, Y. (2009). Inhibition of lipolysis may contribute to the acute regulation of plasma FFA and glucose by FGF21 in ob/ob mice. FEBS Lett. 583:3230–3234.
Rohani-Rasaf, M, Abdollahi, M, Jazayeri, S, Kalantari, N, Asadi-Lari, M. (2013). Correlation of cancer incidence with diet, smoking and socio- economic position across 22 districts of Tehran in 2008. Asian Pac J Cancer Prev. 2013; 14:1669–76. [PubMed: 23679254].
Salehi Nodeh, A, Ghafouri, S, Razavi, S, Mirshafie, SA. (2008). Assessment of TPS tumor marker with ELISA for early detection and monitoring of Breast cancer. Payavard Salamat; 2:84-88.
Tomlinson, E, Fu, L, John, L, Hultgren, B, Huang, X, Renz, M, Stephan, JP, Tsai, SP, Powell-Braxton, L, French, D, Stewart, TA. (2002). Transgenic mice expressing human fibroblast growth factor-19 display increased metabolic rate and decreased adiposity. Endocrinology. 143:1741–1747.
Vasen, HFA, Tomlinson, I, Castells, A. (2015).Clinical management of hereditary colorectal cancer syndromes. Nat Rev Gastroenterol Hepatol. 12:88–97. [PubMed: 25582351].
Warthin, AS. (1913). Heredity with reference to carcinoma: as shown by the study of the cases examined in the pathological laboratory of the University of Michigan. Arch Intern Med. 12:546–55.
Wu, X, Ge, H, Lemon, B, Weiszmann, J, Gupte, J, Hawkins, N, Li, X, Tang, J, Lindberg, R, Li, Y. (2009). Selective activation of FGFR4 by an FGF19 variant does not improve glucose metabolism in ob/ob mice. Proc Natl Acad Sci U S A. 106:14379–14384.
Xu, J, Lloyd, DJ, Hale, C, Stanislaus, S, Chen, M, Sivits, G, Vonderfecht, S, Hecht, R, Li, YS, Lindberg, RA, Chen, JL, Jung, DY, Zhang, Z, Ko, HJ, Kim, JK, Véniant, MM. (2009). Fibroblast growth factor 21 reverses hepatic steatosis, increases energy expenditure, and improves insulin sensitivity in diet-induced obese mice. Diabetes. 58:250–259.
Xu, J, Stanislaus, S, Chinookoswong, N, Lau, YY, Hager, T, Patel, J, Ge, H, Weiszmann, J, Lu, SC, Graham, M, Busby, J, Hecht, R, Li, YS, Li, Y, Lindberg, R, Véniant, MM. (2009). Acute glucose-lowering and insulin-sensitizing action of FGF21 in insulin resistant mouse models—Association with liver and adipose tissue effects. Am J Physiol Endocrinol Metab 297: 1105–1114.