Abstract:
:Extracellular matrix (ECM)-independent survival is an essential prerequisite for tumor metastasis, and a hallmark of epithelial cancer stem cells and epithelial-mesenchymal transition (EMT). Here, we found that loss of TP53I11 enhanced, and overexpression of TP53I11 suppressed the ECM-independent survival, EMT, and migration in MCF10A cells. TP53I11 has long been considered as a transcriptional target of TP53. However, we found that TP53I11 regulated the ECM-independent survival by a TP53-independent way. As a metabolic sensor, AMPK promoted anoikis resistance by inhibiting AKT/m-TOR/p70S6K signaling pathway. It was recently revealed that the reciprocal inhibitory relationship between AKT and AMPK regulated adaptation of cells to ECM-detachment. Our results demonstrated that loss of TP53I11 promoted the activation of AKT/m-TOR pathway, increased PGC-1α expression and thereby enhanced OXPHOS in attach-cultured MCF10A cells, but promoted AMPK activation to inhibit AKT/m-TOR/p70S6K signaling pathway in detach-cultured MCF10A cells. This indicates that TP53I11 functions as a mediator to balance activation of AKT and AMPK to adapt cells to different cellular contexts such as ECM-attachment and -detachment. © 2018 IUBMB Life, 71(1):183-191, 2019.
journal_name
IUBMB Lifejournal_title
IUBMB lifeauthors
Xiao T,Xu Z,Zhou Y,Zhang H,Geng J,Liang Y,Qiao H,Suo Gdoi
10.1002/iub.1949subject
Has Abstractpub_date
2019-02-01 00:00:00pages
183-191issue
2eissn
1521-6543issn
1521-6551journal_volume
71pub_type
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