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000305791 0247_ $$2doi$$a10.1038/s41388-018-0654-9
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000305791 0247_ $$2ISSN$$a0950-9232
000305791 0247_ $$2ISSN$$a1476-5594
000305791 037__ $$aDKFZ-2025-02408
000305791 041__ $$aEnglish
000305791 082__ $$a610
000305791 1001_ $$aGold, Ayala$$b0
000305791 245__ $$aSpironolactone inhibits the growth of cancer stem cells by impairing DNA damage response.
000305791 260__ $$aLondon$$bSpringer Nature$$c2019
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000305791 520__ $$aThe cancer stem cell (CSC) model suggests that a subpopulation of cells within the tumor, the CSCs, is responsible for cancer relapse and metastasis formation. CSCs hold unique characteristics, such as self-renewal, differentiation abilities, and resistance to chemotherapy, raising the need for discovering drugs that target CSCs. Previously we have found that the antihypertensive drug spironolactone impairs DNA damage response in cancer cells. Here we show that spironolactone, apart from inhibiting cancerous cell growth, is also highly toxic to CSCs. Notably, we demonstrate that CSCs have high basal levels of DNA double-strand breaks (DSBs). Mechanistically, we reveal that spironolactone does not damage the DNA but impairs DSB repair and induces apoptosis in cancer cells and CSCs while sparing healthy cells. In vivo, spironolactone treatment reduced the size and CSC content of tumors. Overall, we suggest spironolactone as an anticancer reagent, toxic to both cancer cells and, particularly to, CSCs.
000305791 588__ $$aDataset connected to CrossRef, PubMed, , Journals: inrepo02.dkfz.de
000305791 650_7 $$2NLM Chemicals$$aAntineoplastic Agents
000305791 650_7 $$027O7W4T232$$2NLM Chemicals$$aSpironolactone
000305791 650_2 $$2MeSH$$aAnimals
000305791 650_2 $$2MeSH$$aAntineoplastic Agents: administration & dosage
000305791 650_2 $$2MeSH$$aAntineoplastic Agents: pharmacology
000305791 650_2 $$2MeSH$$aCell Line, Tumor
000305791 650_2 $$2MeSH$$aCell Proliferation
000305791 650_2 $$2MeSH$$aCell Survival: drug effects
000305791 650_2 $$2MeSH$$aDNA Repair: drug effects
000305791 650_2 $$2MeSH$$aDrug Repositioning
000305791 650_2 $$2MeSH$$aHeLa Cells
000305791 650_2 $$2MeSH$$aHumans
000305791 650_2 $$2MeSH$$aMice
000305791 650_2 $$2MeSH$$aNeoplasms: drug therapy
000305791 650_2 $$2MeSH$$aNeoplasms: genetics
000305791 650_2 $$2MeSH$$aNeoplastic Stem Cells: drug effects
000305791 650_2 $$2MeSH$$aSpironolactone: administration & dosage
000305791 650_2 $$2MeSH$$aSpironolactone: pharmacology
000305791 650_2 $$2MeSH$$aXenograft Model Antitumor Assays
000305791 7001_ $$aEini, Lital$$b1
000305791 7001_ $$aNissim-Rafinia, Malka$$b2
000305791 7001_ $$aViner, Ruth$$b3
000305791 7001_ $$aEzer, Shlomit$$b4
000305791 7001_ $$aErez, Keren$$b5
000305791 7001_ $$aAqaqe, Nasma$$b6
000305791 7001_ $$aHanania, Rotem$$b7
000305791 7001_ $$00000-0002-5083-0809$$aMilyavsky, Michael$$b8
000305791 7001_ $$aMeshorer, Eran$$b9
000305791 7001_ $$aGoldberg, Michal$$b10
000305791 773__ $$0PERI:(DE-600)2008404-3$$a10.1038/s41388-018-0654-9$$gVol. 38, no. 17, p. 3103 - 3118$$n17$$p3103 - 3118$$tOncogene$$v38$$x0950-9232$$y2019
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