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. 2022 Oct 12;12:999643. doi: 10.3389/fonc.2022.999643

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Copyright © 2022 Zhou, Lei, Tian, Guo, Chen, Qiu, Wu, Li and Chang

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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The mechanism of cervical cancer radioresistance after radiotherapy. After RT, DNA double strand breaks in cervical cancer cells, and some cancer cells show apoptosis and necrosis, reaching the effect of RT. Other fraction of cancer cells has DNA damage repair (including HR and NHEJ). The wrong repair path leads to the accumulation of acquired mutations, and tumor aggressivity and recurrence, while the correct repair leads to cell survival and radioresistance. CSC, cancer stem cell; HR, homologous recombination; NHEJ, non-homologous end joining; RT, radiotherapy.