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000301746 1001_ $$0P:(DE-He78)0a4c58c6737b30b65df3ed36acc08d4f$$aVelimirovic, Milica$$b0$$eFirst author$$udkfz
000301746 245__ $$aHypoxic HPV-Positive Cancer Cells Are Particularly Sensitive to the Pro-Senescent Effects of B-MYB Repression Due to the Lack of Compensatory A-MYB Induction.
000301746 260__ $$aBognor Regis [u.a.]$$bWiley$$c2025
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000301746 520__ $$aTumor hypoxia is typically linked to increased therapy resistance and poor prognosis of many malignancies, including HPV-positive cancers. One possible resistance mechanism is the increased resistance of hypoxic tumor cells to cellular senescence. It is thus highly interesting to identify strategies which could increase their pro-senescent susceptibility. In comparative analyses of normoxic and hypoxic HPV-positive cancer cells, we here uncover that the interconnection between B-MYB and its paralog A-MYB plays a key role for their senescence response, but shows a differential regulation under normoxia and hypoxia. In specific, we demonstrate that the pro-senescent response to B-MYB loss is counteracted by a compensatory upregulation of A-MYB under normoxia. Therefore, efficient induction of senescence in normoxic cells requires the downregulation of both B-MYB and A-MYB. Interestingly, this compensatory A-MYB induction is absent under hypoxia, rendering hypoxic cancer cells particularly sensitive to the pro-senescent effect of B-MYB repression. We further show that these regulatory effects are not confined to HPV-positive cancer cells, indicating that they could be broadly conserved between different cancer types. Collectively, our findings reveal that hypoxic cancer cells are particularly sensitive to B-MYB inhibition, which could provide a new strategy to target this therapeutically challenging cancer cell population.
000301746 536__ $$0G:(DE-HGF)POF4-314$$a314 - Immunologie und Krebs (POF4-314)$$cPOF4-314$$fPOF IV$$x0
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000301746 650_7 $$2Other$$aA‐MYB
000301746 650_7 $$2Other$$aB‐MYB
000301746 650_7 $$2Other$$acervical cancer
000301746 650_7 $$2Other$$ahuman papillomavirus (HPV)
000301746 650_7 $$2Other$$ahypoxia
000301746 650_7 $$2Other$$asenescence
000301746 650_7 $$2NLM Chemicals$$aTrans-Activators
000301746 650_7 $$2NLM Chemicals$$aMYBL2 protein, human
000301746 650_7 $$2NLM Chemicals$$aMYB protein, human
000301746 650_7 $$2NLM Chemicals$$aCell Cycle Proteins
000301746 650_7 $$2NLM Chemicals$$aProto-Oncogene Proteins c-myb
000301746 650_2 $$2MeSH$$aHumans
000301746 650_2 $$2MeSH$$aCellular Senescence
000301746 650_2 $$2MeSH$$aCell Line, Tumor
000301746 650_2 $$2MeSH$$aTrans-Activators: genetics
000301746 650_2 $$2MeSH$$aTrans-Activators: metabolism
000301746 650_2 $$2MeSH$$aCell Hypoxia
000301746 650_2 $$2MeSH$$aPapillomaviridae
000301746 650_2 $$2MeSH$$aPapillomavirus Infections
000301746 650_2 $$2MeSH$$aCell Cycle Proteins
000301746 650_2 $$2MeSH$$aProto-Oncogene Proteins c-myb
000301746 7001_ $$0P:(DE-He78)b99b271e0ad2dea9ba3ebefc35af9a76$$aAvenhaus, Alicia$$b1$$udkfz
000301746 7001_ $$0P:(DE-He78)2ebb2998d182d99478108ef2cb4b804c$$aLohrey, Claudia$$b2$$udkfz
000301746 7001_ $$0P:(DE-He78)c04ec6ab9480d74da506d656185ec7d2$$aBulkescher, Julia$$b3$$udkfz
000301746 7001_ $$0P:(DE-He78)25779f8829ab7a7650e85a4cc871e6ac$$aHoppe-Seyler, Felix$$b4$$udkfz
000301746 7001_ $$0P:(DE-He78)97468f1980416a4376b44e701d25f24b$$aHoppe-Seyler, Karin$$b5$$eLast author$$udkfz
000301746 773__ $$0PERI:(DE-600)1475090-9$$a10.1002/jmv.70422$$gVol. 97, no. 6, p. e70422$$n6$$pe70422$$tJournal of medical virology$$v97$$x0146-6615$$y2025
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