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MetabolomicsCDK4/6 inhibitor-mediated cell overgrowth triggers an osmotic stress response and chronic p38MAPK activation to promote long-term cell cycle arrest

Cell size and the cell cycle are intrinsically coupled and abnormal increases in cell size are associated with senescence and permanent cell cycle arrest. The mechanism by which overgrowth primes cells to withdraw from the cell cycle remains unknown. We investigate this here using CDK4/6 inhibito...

2025-10-24 | MTBLS5868 | MetaboLights
MetabolomicsX-ray Irradiation Suppresses Keloid Growth by Inducing G2/M Arrest via the Phytosphingosine-KIF20A Axis
Keloid radiotherapy is clinically effective but has an incomplete underlying molecular mechanism and limited accessibility; we used X-ray exposure to identify effector pathways replicating its antifibrotic benefits without further radiation. After collecting patient keloid samples, primary human kel...
2026-06-06 | MTBLS14461 | MetaboLights
MetabolomicsHypoxia Dependent Inhibition of Glioblastoma Cell Proliferation, Invasion, and Metabolism by the Choline-Kinase Inhibitor JAS239
Background: Elevated choline kinase alpha (ChoK) levels are observed in most solid tumors, including glioblastomas (GBM), and ChoK inhibitors have demonstrated limited efficacy in GBM models. Given that hypoxia is associated with resistance to GBM therapy, we hypothesized that tumor hypoxia c...
2024-06-18 | MTBLS6212 | MetaboLights
MetabolomicsCell overgrowth potentiates osmotic and replication stresses to promote p38/p53/p21-dependent senescence
Abnormal increases in cell size are associated with senescence and cell cycle exit. The mechanisms by which overgrowth primes cells to withdraw from the cell cycle remain unknown. We address this question using CDK4/6 inhibitors, which arrest cells in G0/G1 and are licensed to treat advanced HR+/HER...
2025-10-24 | MTBLS8698 | MetaboLights
ProteomicsTEAD inhibitor K-975 enhances KRASG12C inhibitor adagrasib-mediated cancer cell proliferation inhibition via dual cell cycle arrest
Here we investigate the effect of the dual inhibition, in KRASG12C mutated NSCLC cells, using the KRASG12Ci adagrasib (MRTX849) and the pan-TEAD inhibitor (TEADi) K-975. We show that K-975 enhances adagrasib-induced tumor cell growth inhibition in cancer cells. Mechanistically, we detect a downregul...
ORGANISM(S): Homo Sapiens (human) 
2023-05-12 | PXD039726 | JPOST Repository
TranscriptomicsMicroRNA expression during cell cycle arrest
The miR-16 family, which targets genes important for the G1-S transition, is a known modulator of the cell cycle, and members of this family are often deleted or down-regulated in many types of cancers. Here we report the reciprocal relationship - that of the cell cycle controlling the miR-16 family...
ORGANISM(S): Mus musculus 
2011-09-15 | E-GEOD-31225 | biostudies-arrayexpress
ProteomicsProteomic Analysis of the Response to Cell Cycle Arrests in Human Myeloid Leukemia Cells
Previously (Ly et al. 2014), we analyzed protein abundance changes across a ‘minimally perturbed’ cell cycle in human cells (NB4), using centrifugal elutriation to differentially enrich distinct cell cycle phases. Here, we compare data from elutriated cells with NB4 cells arrested at comparable ...
ORGANISM(S): Homo Sapiens (ncbitaxon:9606) 
2017-03-31 | MSV000080841 | MassIVE
TranscriptomicsCoordinated regulation of cell cycle transcripts by p53-inducible microRNAs, miR -192 and -215
Cell cycle arrest in response to DNA damage is an important anti-tumorigenic mechanism. microRNAs (miRNAs) were shown recently to play key regulatory roles in cell cycle progression. For example, miR-34a is induced in response to p53 activation and mediates G1 arrest by down-regulating multiple ce...
ORGANISM(S): Homo sapiens 
2010-06-24 | E-GEOD-13105 | biostudies-arrayexpress
MetabolomicsIFN-γ-driven iNOS induction in macrophages mediates CAR T cell resistance in B cell lymphoma
Chimeric antigen receptor (CAR) T cell therapies have revolutionized B cell malignancy treatment, but subsets of patients with large B cell lymphoma (LBCL) experience primary resistance or relapse after CAR T cell treatment. To uncover tumor microenvironment (TME)-induced resistance mechanisms, we e...
2026-05-31 | MTBLS14634 | MetaboLights
MetabolomicsIFN-γ-driven iNOS induction in macrophages mediates CAR T cell resistance in B cell lymphoma (Glucose Tracer)
Chimeric antigen receptor (CAR) T cell therapies have revolutionized B cell malignancy treatment, but subsets of patients with large B cell lymphoma (LBCL) experience primary resistance or relapse after CAR T cell treatment. To uncover tumor microenvironment (TME)-induced resistance mechanisms, we e...
2026-05-31 | MTBLS14641 | MetaboLights
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