<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Ding L</submitter><funding>Natural Science Foundation of Beijing Municipality</funding><funding>National Natural Science Foundation of China</funding><pagination>875-884</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8403591</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>10(4)</volume><pubmed_abstract>Cervical cancer (CC) is a type of pelvic malignant tumor that severely threatens women's health. Current evidence suggests that &lt;i>IER5&lt;/i>, as a potential radiosensitizer, promotes irradiation-induced apoptosis in CC tissues in patients undergoing chemoradiotherapy. &lt;i>IER5&lt;/i> has been shown to be involved in the G&lt;sub>2&lt;/sub>/M-phase transition. In the present study, we used &lt;i>Cdc25B&lt;/i> as the breakthrough point to explore the underlying mechanism of &lt;i>IER5&lt;/i> in the cell cycle regulation of radiation-damaged HeLa cells. &lt;i>IER5&lt;/i> was evidently upregulated after irradiation, but &lt;i>Cdc25B&lt;/i> was significantly downregulated. In monoclonal &lt;i>IER5&lt;/i>-silenced HeLa cells, irradiation-induced downregulation of &lt;i>Cdc25B&lt;/i> was attenuated. The effect of irradiation on &lt;i>Cdc25B&lt;/i> </pubmed_abstract><journal>Toxicology research</journal><pubmed_title>&lt;i>Cdc25B&lt;/i> is transcriptionally inhibited by &lt;i>IER5&lt;/i> through the &lt;i>NF-YB&lt;/i> transcription factor in irradiation-treated HeLa cells.</pubmed_title><pmcid>PMC8403591</pmcid><funding_grant_id>31640022</funding_grant_id><funding_grant_id>31770907</funding_grant_id><funding_grant_id>7172146</funding_grant_id><pubmed_authors>Liu X</pubmed_authors><pubmed_authors>Zhou P</pubmed_authors><pubmed_authors>Jiang X</pubmed_authors><pubmed_authors>Xiong Q</pubmed_authors><pubmed_authors>Ding K</pubmed_authors><pubmed_authors>Ding L</pubmed_authors><pubmed_authors>Zhao X</pubmed_authors></additional><is_claimable>false</is_claimable><name>&lt;i>Cdc25B&lt;/i> is transcriptionally inhibited by &lt;i>IER5&lt;/i> through the &lt;i>NF-YB&lt;/i> transcription factor in irradiation-treated HeLa cells.</name><description>Cervical cancer (CC) is a type of pelvic malignant tumor that severely threatens women's health. Current evidence suggests that &lt;i>IER5&lt;/i>, as a potential radiosensitizer, promotes irradiation-induced apoptosis in CC tissues in patients undergoing chemoradiotherapy. &lt;i>IER5&lt;/i> has been shown to be involved in the G&lt;sub>2&lt;/sub>/M-phase transition. In the present study, we used &lt;i>Cdc25B&lt;/i> as the breakthrough point to explore the underlying mechanism of &lt;i>IER5&lt;/i> in the cell cycle regulation of radiation-damaged HeLa cells. &lt;i>IER5&lt;/i> was evidently upregulated after irradiation, but &lt;i>Cdc25B&lt;/i> was significantly downregulated. In monoclonal &lt;i>IER5&lt;/i>-silenced HeLa cells, irradiation-induced downregulation of &lt;i>Cdc25B&lt;/i> was attenuated. The effect of irradiation on &lt;i>Cdc25B&lt;/i> </description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Aug</publication><modification>2026-04-08T08:43:32.246Z</modification><creation>2022-08-04T07:10:47.385Z</creation></dates><accession>S-EPMC8403591</accession><cross_references><pubmed>34484679</pubmed><doi>10.1093/toxres/tfab069</doi></cross_references></HashMap>