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A high-throughput screen identifies that CDK7 activates glucose consumption in lung cancer cells.

Abstract：

:Elevated glucose consumption is fundamental to cancer, but selectively targeting this pathway is challenging. We develop a high-throughput assay for measuring glucose consumption and use it to screen non-small-cell lung cancer cell lines against bioactive small molecules. We identify Milciclib that blocks glucose consumption in H460 and H1975, but not in HCC827 or A549 cells, by decreasing SLC2A1 (GLUT1) mRNA and protein levels and by inhibiting glucose transport. Milciclib blocks glucose consumption by targeting cyclin-dependent kinase 7 (CDK7) similar to other CDK7 inhibitors including THZ1 and LDC4297. Enhanced PIK3CA signaling leads to CDK7 phosphorylation, which promotes RNA Polymerase II phosphorylation and transcription. Milciclib, THZ1, and LDC4297 lead to a reduction in RNA Polymerase II phosphorylation on the SLC2A1 promoter. These data indicate that our high-throughput assay can identify compounds that regulate glucose consumption and that CDK7 is a key regulator of glucose consumption in cells with an activated PI3K pathway.

journal_name

Nat Commun

journal_title

Nature communications

authors

Ghezzi C,Wong A,Chen BY,Ribalet B,Damoiseaux R,Clark PM

doi

10.1038/s41467-019-13334-8

subject

Has Abstract

pub_date

2019-11-29 00:00:00

pages

5444

issue

1

issn

2041-1723

pii

10.1038/s41467-019-13334-8

journal_volume

10

pub_type

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