Home > Publications database > Hypoxic 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. > print |
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024 | 7 | _ | |a 10.1002/jmv.70422 |2 doi |
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024 | 7 | _ | |a 1096-9071 |2 ISSN |
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041 | _ | _ | |a English |
082 | _ | _ | |a 610 |
100 | 1 | _ | |a Velimirovic, Milica |0 P:(DE-He78)0a4c58c6737b30b65df3ed36acc08d4f |b 0 |e First author |u dkfz |
245 | _ | _ | |a Hypoxic 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. |
260 | _ | _ | |a Bognor Regis [u.a.] |c 2025 |b Wiley |
336 | 7 | _ | |a article |2 DRIVER |
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336 | 7 | _ | |a Journal Article |b journal |m journal |0 PUB:(DE-HGF)16 |s 1748871428_11125 |2 PUB:(DE-HGF) |
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520 | _ | _ | |a Tumor 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. |
536 | _ | _ | |a 314 - Immunologie und Krebs (POF4-314) |0 G:(DE-HGF)POF4-314 |c POF4-314 |f POF IV |x 0 |
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650 | _ | 7 | |a A‐MYB |2 Other |
650 | _ | 7 | |a B‐MYB |2 Other |
650 | _ | 7 | |a cervical cancer |2 Other |
650 | _ | 7 | |a human papillomavirus (HPV) |2 Other |
650 | _ | 7 | |a hypoxia |2 Other |
650 | _ | 7 | |a senescence |2 Other |
650 | _ | 7 | |a Trans-Activators |2 NLM Chemicals |
650 | _ | 7 | |a MYBL2 protein, human |2 NLM Chemicals |
650 | _ | 7 | |a MYB protein, human |2 NLM Chemicals |
650 | _ | 7 | |a Cell Cycle Proteins |2 NLM Chemicals |
650 | _ | 7 | |a Proto-Oncogene Proteins c-myb |2 NLM Chemicals |
650 | _ | 2 | |a Humans |2 MeSH |
650 | _ | 2 | |a Cellular Senescence |2 MeSH |
650 | _ | 2 | |a Cell Line, Tumor |2 MeSH |
650 | _ | 2 | |a Trans-Activators: genetics |2 MeSH |
650 | _ | 2 | |a Trans-Activators: metabolism |2 MeSH |
650 | _ | 2 | |a Cell Hypoxia |2 MeSH |
650 | _ | 2 | |a Papillomaviridae |2 MeSH |
650 | _ | 2 | |a Papillomavirus Infections |2 MeSH |
650 | _ | 2 | |a Cell Cycle Proteins |2 MeSH |
650 | _ | 2 | |a Proto-Oncogene Proteins c-myb |2 MeSH |
700 | 1 | _ | |a Avenhaus, Alicia |0 P:(DE-He78)b99b271e0ad2dea9ba3ebefc35af9a76 |b 1 |u dkfz |
700 | 1 | _ | |a Lohrey, Claudia |0 P:(DE-He78)2ebb2998d182d99478108ef2cb4b804c |b 2 |u dkfz |
700 | 1 | _ | |a Bulkescher, Julia |0 P:(DE-He78)c04ec6ab9480d74da506d656185ec7d2 |b 3 |u dkfz |
700 | 1 | _ | |a Hoppe-Seyler, Felix |0 P:(DE-He78)25779f8829ab7a7650e85a4cc871e6ac |b 4 |u dkfz |
700 | 1 | _ | |a Hoppe-Seyler, Karin |0 P:(DE-He78)97468f1980416a4376b44e701d25f24b |b 5 |e Last author |u dkfz |
773 | _ | _ | |a 10.1002/jmv.70422 |g Vol. 97, no. 6, p. e70422 |0 PERI:(DE-600)1475090-9 |n 6 |p e70422 |t Journal of medical virology |v 97 |y 2025 |x 0146-6615 |
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