¹²⁵I Seeds Irradiation To Influence The Expression Of Proliferation And EGFR Of Colorectal Cancer Cells HCT-116 In Vitro

Objective:The aim of our work is to explore the effect and mechanism of continuous irradiation by125I seeds at different dose, in order to restrain growth, induce apoptosis and expression of EGFR of human colorectal cancer cell HCT-116. Methods:The study of irradiation damage to tumor cell was operated in vitro. The irradiator consists of three 125I (Model 6711) seed groups of different average apparent activity at respective 14.53 MBq (0.4mCi),22.97MBq(0.6 mCi),29.97 MB q(0.8 mCi), each group having nine 125I seeds at the same dose. Eight seeds were equally laid around the circumference of diameter 3 cm and the ninth seed was confined to the center for each group. Human colorectal cancer cell HCT-116 were placed 6 mm above the seed plane to accept continuous irradiation lasting for 72 hours.The total delivered dose was 113cGy,162cGy,225cGy respectively, meanwhile the control group without 125I seed irradiation. The expressions of CyclinDl were detected by RT-PCR and the cell growth condition was analyzed by cytometry. The rates of apoptosis and expression of EGFR were determined by flow cytometry.Results:After being irradiated for 72 hours, the growth rate of the HCT-116 cell stepped down dramatically comparing to the control group (P<0.05). Flow cytometry showed that the apoptosis rate was greatly increased compared with the control (P<0.05), and so was the expression of EGFR. The expressions of CyclinDl enhanced in the two high-dose groups at 0.6 mCi and 0.8 mCi. Conclusions:Therefore we can draw the conclusion that with the 125I dose increasing, the growth rate of HCT-116 cell declined and the apoptosis raised dramatically. However, the expression of CyclinD1 was strengthened in the high dose group too, which is related to radiation resistance, as well as EGFR expression raised that is related to cancer recurrence and metastasis,. As a result, continuous low dose irradiation of 125I seeds, in combination with the control of expression of EGFR will enforce the induction of apoptosis and the effectiveness of therapy in colorectal cancer.