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Article: Single-Hit Inactivation Drove Tumor Suppressor Genes Out of the X Chromosome during Evolution

TitleSingle-Hit Inactivation Drove Tumor Suppressor Genes Out of the X Chromosome during Evolution
Authors
Issue Date2022
Citation
Cancer Research, 2022, v. 82, n. 8, p. 1482-1491 How to Cite?
AbstractCancer-related genes are under intense evolutionary pressure. In this study, we conjecture that X-linked tumor suppressor genes (TSG) are not protected by the Knudson's two-hit mechanism and are therefore subject to negative selection. Accordingly, nearly all mammalian species exhibited lower TSG-to-noncancer gene ratios on their X chromosomes compared with nonmammalian species. Synteny analysis revealed that mammalian X-linked TSGs were depleted shortly after the emergence of the XY sex-determination system.Aphylogeny-basedmodel unveiled a higher Xchromosometo- autosome relocation flux for human TSGs. This was verified in other mammals by assessing the concordance/discordance of chromosomal locations of mammalian TSGs and their orthologs in Xenopus tropicalis. In humans, X-linked TSGs are younger or larger in size. Consistently, pan-cancer analysis revealed more frequent nonsynonymous somatic mutations of X-linked TSGs. These findings suggest that relocation of TSGs out of the X chromosome could confer a survival advantage by facilitating evasion of single-hit inactivation.
Persistent Identifierhttp://hdl.handle.net/10722/330793
ISSN
2023 Impact Factor: 12.5
2023 SCImago Journal Rankings: 3.468
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorWang, Xiansong-
dc.contributor.authorHu, Wei-
dc.contributor.authorLi, Xiangchun-
dc.contributor.authorHuang, Dan-
dc.contributor.authorLi, Qing-
dc.contributor.authorChan, Hung-
dc.contributor.authorZeng, Judeng-
dc.contributor.authorXie, Chuan-
dc.contributor.authorChen, Huarong-
dc.contributor.authorLiu, Xiaodong-
dc.contributor.authorGin, Tony-
dc.contributor.authorWang, Maggie Haitian-
dc.contributor.authorCheng, Alfred Sze Lok-
dc.contributor.authorKang, Wei-
dc.contributor.authorTo, Ka Fai-
dc.contributor.authorPlewczynski, Dariusz-
dc.contributor.authorZhang, Qingpeng-
dc.contributor.authorChen, Xiaoting-
dc.contributor.authorChan, Danny Cheuk Wing-
dc.contributor.authorKo, Ho-
dc.contributor.authorWong, Sunny Hei-
dc.contributor.authorYu, Jun-
dc.contributor.authorChan, Matthew Tak Vai-
dc.contributor.authorZhang, Lin-
dc.contributor.authorWu, William Ka Kei-
dc.date.accessioned2023-09-05T12:14:26Z-
dc.date.available2023-09-05T12:14:26Z-
dc.date.issued2022-
dc.identifier.citationCancer Research, 2022, v. 82, n. 8, p. 1482-1491-
dc.identifier.issn0008-5472-
dc.identifier.urihttp://hdl.handle.net/10722/330793-
dc.description.abstractCancer-related genes are under intense evolutionary pressure. In this study, we conjecture that X-linked tumor suppressor genes (TSG) are not protected by the Knudson's two-hit mechanism and are therefore subject to negative selection. Accordingly, nearly all mammalian species exhibited lower TSG-to-noncancer gene ratios on their X chromosomes compared with nonmammalian species. Synteny analysis revealed that mammalian X-linked TSGs were depleted shortly after the emergence of the XY sex-determination system.Aphylogeny-basedmodel unveiled a higher Xchromosometo- autosome relocation flux for human TSGs. This was verified in other mammals by assessing the concordance/discordance of chromosomal locations of mammalian TSGs and their orthologs in Xenopus tropicalis. In humans, X-linked TSGs are younger or larger in size. Consistently, pan-cancer analysis revealed more frequent nonsynonymous somatic mutations of X-linked TSGs. These findings suggest that relocation of TSGs out of the X chromosome could confer a survival advantage by facilitating evasion of single-hit inactivation.-
dc.languageeng-
dc.relation.ispartofCancer Research-
dc.titleSingle-Hit Inactivation Drove Tumor Suppressor Genes Out of the X Chromosome during Evolution-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1158/0008-5472.CAN-21-3458-
dc.identifier.pmid35247889-
dc.identifier.scopuseid_2-s2.0-85128469757-
dc.identifier.volume82-
dc.identifier.issue8-
dc.identifier.spage1482-
dc.identifier.epage1491-
dc.identifier.eissn1538-7445-
dc.identifier.isiWOS:000791529000001-

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