Abstract
BackgroundWe have previously found there was a small subpopulation of cells with cancer stem cell-like phenotype ALDH-1 in cervical cancer. Radiotherapy has been applied in most of the cervical cancer. However,the mechanisms underlying radioresistance still remained elusive. Our study is to explore whether ALDH+ cell promotes radioresistance by hypoxia.MethodsCells were respectively cultured in hypoxia and normoxia environment and analyzed for marker stability, and cell cycle distribution. Results: Cell growth, apoptosis, cell cycle, sphere formation were affected by hypoxia. ALDH-1 and CHK2 were upregulated after hypoxia.ConclusionsHere we show that ALDH-1 positive cells contribute to cervical carcinoma radioresistance through preferential activation of the DNA damage checkpoint response and an increase in DNA repair capacity. The fraction of these cells is enriched after radiation in cervical carcinoma.
Highlights
We have previously found there was a small subpopulation of cells with cancer stem cell-like phenotype Aldehyde dehydrogenase 1 (ALDH-1) in cervical cancer
Hypoxia could generate reactive oxygen species and change the expression of proteins related to the repair of double stranded Deoxyribonucleic acid (DNA) and dysregulating cell cycle checkpoint control leading to an abnormal DNA repair pathways [8,9,10]
We found cervical cancer contains a small subpopulation of cells which may be associated with a cancer stem cell-like phenotype ALDH-1
Summary
We have previously found there was a small subpopulation of cells with cancer stem cell-like phenotype ALDH-1 in cervical cancer. Our study is to explore whether ALDH+ cell promotes radioresistance by hypoxia. Hypoxia could generate reactive oxygen species and change the expression of proteins related to the repair of double stranded DNA and dysregulating cell cycle checkpoint control leading to an abnormal DNA repair pathways [8,9,10]. These various effects related to hypoxia may help protect and maintain the cancer stem cell phenotype, thereby promoting tumor recurrence after treatment [11]
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