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Chorna I.V., Shkandala A.Yu., second-year student
Sumy State University, department of biochemistry and pharmacology
Ionizing radiation remains an effective tool in cancer therapy, but considerable differences exist in the
outcomes of the radiotherapeutic treatment of tumors of different histological origin. Better understanding of the
molecular mechanisms involved in tumor response to ionizing radiation exposure is important for improving
radiotherapy efficiency. Besides, a cross-resistance of tumor cells to anti-cancer drugs and ionizing radiation may
also exist. The mechanisms of such cross-resistance are poorly studied.
The aim of the study was to compare the effect of X-irradiation on growth and apoptosis of cancer cells of
different lines (MCF-7 and T-47D breast cancer cells, K562 human myelogenous leukemia cell line, A549 human
lung adenocarcinoma cells).
It was found that a single 1.5, 3.0 or 4.5 Gy X-ray dose inhibited to a variable extent growth of all cell lines
tested 48h after the radiation treatment. A549 cells presented a higher radiosensitivity compared with other cell
lines. The obtained results showed relative radioresistance of human breast cancer MCF-7 cells in comparison with
T-47D breast cancer cells. Besides, it was revealed a higher proliferative rate in T-47D cells compared to MCF-7
cells. In order to determine whether a decrease in cell number was caused by reducing of proliferative potential of
the cells or by their death, both cell number and proportion of dead cells were counted. It was found that in the case
of MCF-7, T-47D and K562 cells a decrease in cell number after the radiation exposure was caused by a reduction
in their proliferative capacity and delay in G1 phase of cell cycle rather than by cell death. On the contrary, in the
case of A549 cells a decrease in cell number (on 31%, 69% and 84% after irradiation with a dose of 1.5, 3.0 and 4.5
Gy, correspondingly) was caused by their death.
Thus, tumour cells are highly adapted for survival and proliferation. They can successfully survive after
natural and artificial (therapeutic) selection by producing new variants. A better understanding of tumour
heterogeneity will help scientists to clarify such important biological phenomena as drug resistance, spontaneous
regression and will be able to improve cancer prevention, diagnosis and therapy.