• Low molecular weight b-FGF supplementation causes the HT29 colon cancer cell line more susceptible to apoptosis resistance.
  • Hosein Jodat,1,* Zari Tahan Nejad Asadi,2 Dian Dayer,3 Nasrin Amirrajab,4
    1. Department of Laboratory Sciences, School of Allied Medical Sciences, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
    2. Thalassemia and Hemoglobinopathy Research Center, Research Institute of Health, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
    3. Cellular and Molecular Research Center, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
    4. Infectious and Tropical Diseases Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran


  • Introduction: Basic fibroblast growth factor (bFGF) is a signaling molecule involved in tissue regeneration, cell proliferation, and morphogenesis. Some studies claim that bFGF is necessary for the development, distribution, and development of tumors. However, other studies have revealed that bFGF causes cancer cells to undergo apoptosis. This investigation aimed to investigate bFGF's impact on the development and survival of the HT29 colorectal cell line.
  • Methods: HT29 cells were treated with 25 ng/mL of 18 KD bFGF for 48 h. Cell viability was determined using MTT assay. A clonogenic assay was performed using crystal violet staining. The gene expression was investigated using the Real-Time PCR method.
  • Results: Different concentrations of bFGF had no toxic effect on HT29 cells (P > 0.05). The viability of the bFGF-treated cells was higher than control cells. However, the difference was not significant ( P > 0.05). The ability of clonogenicity in the bFGF-treated group was not significantly different from the control group (P = 0.1039). The expression of Bax in the bFGF-treated group showed a significant decrease compared to the control group (P = 0.0046). However, the expression of BCl-2 was significantly increased in the bFGF-treated group (P = 0.0011). The bFGF therapy decreased the expression of Caspase 3 while increasing the expression of CyclinD1 and Survivin. Even though they were not statistically significant (P = 0.1899, 0.1204 and 0.1586 respectively).
  • Conclusion: The bFGF can be considered as an inducer of proliferation that provides resistance to apoptosis in the HT29 colorectal cell line.
  • Keywords: Colorectal Cancer, bFGF, apoptosis, HT29 cell line