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Chk1 inhiitors decrease the expressions of STAT3 downstream target genes in multiple myeloma cells

ABSTRACT: Chk1 inhiitors decrease the expressions of STAT3 downstream target genes in multiple myeloma cells

PROVIDER: PRJNA730521 | ENA |

REPOSITORIES: ENA

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Chk1 inhiitors decrease the expressions of STAT3 downstream target genes in multiple myeloma cells

Project description:Study #1: U266 cells were treated with 100 nM PF477736 for 4 hr. Study #2: U266 cells were treated with 100 nM PF477736 for 16 hr. Study #3: KAS/6-1 cells were treated with 50 nM PF477736 or 300 nM CEP3891 for 2 hr.

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Project description:While effective anti-cancer drugs targeting the CHK1 kinase are advancing in the clinic, drug resistance is rapidly emerging. Here, we demonstrate that CRISPR-mediated knockout of the little-known gene FAM122A confers cellular resistance to CHK1 inhibitors and cross-resistance to ATR inhibitors. Knockout of FAM122A results in activation of PP2A-B55α, a phosphatase which dephosphorylates the WEE1 protein and rescues WEE1 from Ubiquitin-mediated degradation. The resulting increase in WEE1 protein expression reduces replication stress, activates the G2/M checkpoint, and confers cellular resistance to CHK1 inhibitors. Interestingly, in tumor cells with oncogene-driven replication stress, CHK1 can directly phosphorylate FAM122A, leading to activation of the PP2A-B55α phosphatase and increased WEE1 expression. A combination of a CHK1 inhibitor plus a WEE1 inhibitor can overcome CHK1 inhibitor resistance of these tumor cells, thereby enhancing anti-cancer activity. The FAM122A expression level in a tumor cell can serve as a useful biomarker for predicting CHK1 inhibitor sensitivity or resistance.

2021-01-01 | GSE158338 | GEO

Identify the downstream targets of Stat3 by using an engineered mouse ES cell line treated with GCSF and LIF plus PD0325901

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Identify the downstream targets of Stat3 by using an engineered mouse ES cell line treated with GCSF and LIF plus PD0325901

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