Enhanced autophagy in colorectal cancer stem cells does not contribute to radio-resistance

Autophagy, an essential catabolic pathway of degrading cellular components within the lysosome, has been found to benefit the growth and therapeutic resistance of cancer cells. In this study, we investigated the role of autophagy in the radiosensitivity of cancer stem cells. By separating CD44(+)/CD133(+) cancer stem cells from parental HCT8 human colorectal cancer cells, we found a significantly higher level of autophagy in the CD44(+)/CD133(+) cells than in the parental cells. Exposure to 5 Gy of eta-ray significantly damaged both CD44(+)/CD133(+) cells and parental cells, but the radiation-induced damage did not differ between the groups. Unexpectedly, autophagy was not significantly induced by radiation exposure in the CD44(+)/CD133(+) cells and parental cells. The inhibition of autophagy by the silencing of ATG7, a factor required for autophagy at the stage of autophagosome precursor synthesis, did not significantly change the growth and radiation-induced damage in both CD44(+)/CD133(+) cells and parental cells. Although an enhanced basic level of autophagy was found in the CD44(+)/CD133(+) cancer stem cells, our data suggest that the canonical autophagy in cancer cells plays few roles, if any, in radio-sensitivity.