Enhanced Kat3A/Catenin transcription: a common mechanism of therapeutic resistance.
CREB-binding protein
Kat3 coactivator
cancer stem cell
p300
stem cell
therapy resistance
Journal
Cancer drug resistance (Alhambra, Calif.)
ISSN: 2578-532X
Titre abrégé: Cancer Drug Resist
Pays: United States
ID NLM: 101738710
Informations de publication
Date de publication:
2019
2019
Historique:
entrez:
20
5
2020
pubmed:
1
1
2019
medline:
1
1
2019
Statut:
ppublish
Résumé
Cancers are heterogeneous at the cellular level. Cancer stem cells/tumor initiating cells (CSC/TIC) both initiate tumorigenesis and are responsible for therapeutic resistance and disease relapse. Elimination of CSC/TIC should therefore be able to reverse therapy resistance. In principle, this could be accomplished by either targeting cancer stem cell surface markers or "stemness" pathways. Although the successful therapeutic elimination of "cancer stemness" is a critical goal, it is complex in that it should be achieved without depletion of or increases in somatic mutations in normal tissue stem cell populations. In this perspective, we will discuss the prospects for this goal via pharmacologically targeting differential Kat3 coactivator/Catenin usage, a fundamental transcriptional control mechanism in stem cell biology.
Identifiants
pubmed: 32426696
doi: 10.20517/cdr.2019.32
pmc: PMC7234864
mid: NIHMS1588276
doi:
Types de publication
Journal Article
Langues
eng
Pagination
917-932Subventions
Organisme : NCI NIH HHS
ID : R01 CA166161
Pays : United States
Organisme : NINDS NIH HHS
ID : R21 NS074392
Pays : United States
Organisme : NCI NIH HHS
ID : U54 CA209978
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA014089
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL112638
Pays : United States
Organisme : NIAID NIH HHS
ID : R21 AI105057
Pays : United States
Déclaration de conflit d'intérêts
Conflicts of interest All authors declared that there are no conflicts of interest.
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