Radiation promotes malignant phenotypes through SRC in breast cancer cells.
Bottom Line: However, the molecular mechanisms underlying radiation-induced cancer progression remain obscure.Importantly, radiation-activated SRC induced SLUG expression and caused epithelial-mesenchymal cell transition through phosphatidylinositol 3-kinase/protein kinase B and p38 MAPK signaling.In addition, downregulation of SRC also abolished radiation-acquired resistance of breast cancer cells to anticancer agents such as cisplatin, etoposide, paclitaxel, and IR.
Affiliation: Department of Life Science, Research Institute for Natural Sciences, Hanyang University, Seoul, Korea.Show MeSH
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Mentions: As EMT is often associated with the CSC population, we examined whether radiation-activated SRC is also involved in expansion of the CSC population. To this end, we analyzed the CD44+/CD24− cell population in both MCF7 and SKBR3 breast cancer cells after exposure to a single dose (6 Gy) or fractionated dose (2 Gy ×3) of radiation. Notably, irradiation caused an increase in the CD44+/CD24− cell population, well-known as CSCs in breast cancer (Fig.4a). Intriguingly, fractionated irradiation had more effect on the increase of CD44+/CD24− cells compared to single irradiation, although irradiated doses were equal. However, treatment with siRNA targeting SRC suppressed the radiation-induced expansion of CD44+ cells to basal levels (Fig.4b).
Affiliation: Department of Life Science, Research Institute for Natural Sciences, Hanyang University, Seoul, Korea.