An acetyl-histone vulnerability in PI3K/AKT inhibition-resistant cancers is targetable by both BET and HDAC inhibitors

Acquisition of resistance to phosphatidylinositol 3-kinase (PI3K)/AKT-targeted monotherapy implies the existence of common resistance mechanisms independent of cancer type. Here, we demonstrate that PI3K/AKT inhibitors cause glycolytic crisis, acetyl-coenzyme A (CoA) shortage, and a global decrease...

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Veröffentlicht in:	Cell reports (Cambridge) 2021-02, Vol.34 (7), p.108744-108744, Article 108744
Hauptverfasser:	Wu, Di, Yan, Yuqian, Wei, Ting, Ye, Zhenqing, Xiao, Yutian, Pan, Yunqian, Orme, Jacob J., Wang, Dejie, Wang, Liguo, Ren, Shancheng, Huang, Haojie
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Cell Line, Tumor Cell Proliferation - drug effects Drug Resistance, Neoplasm HCT116 Cells Histone Deacetylase Inhibitors - pharmacology Histones - metabolism Humans Male Mice Mice, SCID Neoplasms - drug therapy Neoplasms - enzymology Neoplasms - metabolism Nerve Tissue Proteins - antagonists & inhibitors Nerve Tissue Proteins - metabolism Phosphatidylinositol 3-Kinases - metabolism Phosphoinositide-3 Kinase Inhibitors - pharmacology Proto-Oncogene Proteins c-akt - antagonists & inhibitors Proto-Oncogene Proteins c-akt - metabolism Receptors, Cell Surface - antagonists & inhibitors Receptors, Cell Surface - metabolism Xenograft Model Antitumor Assays
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