https://transhumanist.ru/index.php?action=history&feed=atom&title=EID3EID3 - История изменений2026-04-19T12:58:17ZИстория изменений этой страницы в викиMediaWiki 1.43.6https://transhumanist.ru/index.php?title=EID3&diff=4357&oldid=prevOdysseusBot: Новая страница: «EP300-interacting inhibitor of differentiation 3 (EID-3) (E1A-like inhibitor of differentiation 3) (EID-1-like inhibitor of differentiation 3) (Non-structural mai...»2021-04-29T19:14:02Z<p>Новая страница: «EP300-interacting inhibitor of differentiation 3 (EID-3) (E1A-like inhibitor of differentiation 3) (EID-1-like inhibitor of differentiation 3) (Non-structural mai...»</p>
<p><b>Новая страница</b></p><div>EP300-interacting inhibitor of differentiation 3 (EID-3) (E1A-like inhibitor of differentiation 3) (EID-1-like inhibitor of differentiation 3) (Non-structural maintenance of chromosomes element 4 homolog B) (NS4EB) (Non-SMC element 4 homolog B)<br />
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==Publications==<br />
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{{medline-entry<br />
|title=Upregulation of [[EID3]] sensitizes breast cancer cells to ionizing radiation-induced cellular senescence.<br />
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/30114644<br />
|abstract=Previous studies have shown that BMS-345541 (BMS, a specific IκB kinase β inhibitor) sensitized various tumor cells including MCF-7 breast cancer cells to ionizing radiation (IR). However, the mechanisms of BMS action are unknown. Since the expression of E1A-like inhibitor of differentiation 3 ([[EID3]]) was highly upregulated in MCF-7 cells after BMS treatment, we investigated the role of [[EID3]] in the response of MCF-7 cells to IR. We found that BMS induced [[EID3]] expression in MCF-7 cells in a time- and dose-dependent manner. Knockdown of [[EID3]] by specific shRNA attenuated BMS-induced radiosensitization in MCF-7 cells. In contrast, induction of [[EID3]] expression in an inducible [[EID3]] expressing MCF-7 cell line with doxycycline sensitized the cells to IR. [[EID3]]-mediated sensitization of MCF-7 cells to IR was not attributed to an increase in apoptosis. Instead, [[EID3]]-expressing MCF-7 cells exhibited significantly higher levels of senescence associated β-galactosidase (SA-β-gal) activity and higher levels of p21 and p57 than [[EID3]]-MCF-7 cells without induction of [[EID3]] after exposure to IR. Similar findings were observed when [[EID3]]-expressing MCF-7 cells were treated with etoposide, a topoisomerase II inhibitor. Taken together, our findings reveal a novel function of [[EID3]] and suggest that the induction of [[EID3]] by BMS may be exploited as a new strategy to sensitize breast cancer cells to IR and chemotherapy by inducing cancer cell senescence.<br />
|mesh-terms=* Breast Neoplasms<br />
* Carrier Proteins<br />
* Cellular Senescence<br />
* Cyclin-Dependent Kinase Inhibitor Proteins<br />
* DNA Damage<br />
* DNA Repair<br />
* Etoposide<br />
* Female<br />
* Gene Expression Regulation, Neoplastic<br />
* Gene Knockdown Techniques<br />
* HEK293 Cells<br />
* Humans<br />
* Imidazoles<br />
* MCF-7 Cells<br />
* Quinoxalines<br />
* Radiation, Ionizing<br />
* Radiation-Sensitizing Agents<br />
* Time Factors<br />
* Up-Regulation<br />
|keywords=* Chemotherapy<br />
* EID3<br />
* Ionizing<br />
* MCF-7 breast cancer cells<br />
* Radiation<br />
* Senescence<br />
|full-text-url=https://sci-hub.do/10.1016/j.biopha.2018.08.022<br />
}}</div>OdysseusBot