Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Loss of the lipid transfer protein STARD7 triggers metabolic reprogramming and an epigenetic-mediated cell cycle arrest in breast cancer

ABSTRACT: Loss of the lipid transfer protein STARD7 triggers metabolic reprogramming and an epigenetic-mediated cell cycle arrest in breast cancer

PROVIDER: PRJNA1055592 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Loss of the lipid transfer protein STARD7 triggers metabolic reprogramming and an epigenetic-mediated cell cycle arrest in breast cancer

Project description:Cancer cells have to constantly adapt their metabolism to support aberrant cell proliferation. However, the functional link between metabolic reprogramming and cell cycle progression remain largely unexplored. Mitochondria rely on the transfer of multiple lipids from the endoplasmic reticulum (ER) to their membranes to be functional. Several mitochondrial-derived metabolites influence cancer cell proliferation by modulating the epigenome. Here we show that the loss of STARD7, a lipid transfer protein whose expression is enhanced in breast cancer, leads to a profound metabolic reprogramming characterized by the increased synthesis of Carnitine derivatives and S-Adenosyl-L-methionine (SAM). Elevated SAM levels causes the accumulation of H3K27 trimethylation, a repressive mark, on many gene promoters coding for candidates involved in cell cycle progression and in the response to oxidative stress. As a result, STARD7 deficiency triggers cell cycle arrest, at least through defective ERa- and EGFR-dependent signaling pathways as well as to autophagy and ciliogenesis. Collectively, our data define STARD7 as a critical candidate involved in cell cycle progression in breast cancer.

2025-09-03 | GSE251873 | GEO

Loss of the lipid transfer protein STARD7 triggers metabolic reprogramming and an epigenetic-mediated cell cycle arrest in breast cancer

Project description:Cancer cells have to constantly adapt their metabolism to support aberrant cell proliferation. However, the functional link between metabolic reprogramming and cell cycle progression remain largely unexplored. Mitochondria rely on the transfer of multiple lipids from the endoplasmic reticulum (ER) to their membranes to be functional. Several mitochondrial-derived metabolites influence cancer cell proliferation by modulating the epigenome. Here we show that the loss of STARD7, a lipid transfer protein whose expression is enhanced in breast cancer, leads to a profound metabolic reprogramming characterized by the increased synthesis of Carnitine derivatives and S-Adenosyl-L-methionine (SAM). Elevated SAM levels causes the accumulation of H3K27 trimethylation, a repressive mark, on many gene promoters coding for candidates involved in cell cycle progression and in the response to oxidative stress. As a result, STARD7 deficiency triggers cell cycle arrest, at least through defective ER?- and EGFR-dependent signaling pathways as well as to autophagy and ciliogenesis. Collectively, our data define STARD7 as a critical candidate involved in cell cycle progression in breast cancer.

2025-09-01 | PXD046984 | Pride

Loss of KNTC1 Triggers a 53BP1 and USP28 Dependent Cell Cycle Arrest Without Prolonged Mitotic Delays

Project description:Loss of KNTC1 Triggers a 53BP1 and USP28 Dependent Cell Cycle Arrest Without Prolonged Mitotic Delays

| PRJNA1309730 | ENA

MESH1 knockdown triggers proliferation arrest through TAZ repression

Project description:MESH1 knockdown triggers proliferation arrest through TAZ repression

| PRJNA612863 | ENA

MicroRNA expression during cell cycle arrest

Project description: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. Levels of this family increase rapidly as cells are arrested in G0. Conversely, as cells are released from G0 arrest, levels of the miR-16 family rapidly decrease. Such rapid changes are made possible by the unusual instabilities of several family members. The repression mediated by the miR-16 family is sensitive to these cell cycle changes, which suggests that the rapid up-regulation of the miR-16 family reinforces cell cycle arrest in G0. Upon cell cycle re-entry, the rapid decay of several members allows levels of the family to decrease, alleviating repression of target genes and allowing proper resumption of the cell cycle. Small RNAs were profiled by high-throughput sequencing either during synchronous release after serum starvation or during cell-cycle arrest by contact inhibition.

2011-09-15 | E-GEOD-31225 | biostudies-arrayexpress

CDK4/6 inhibitor-mediated cell overgrowth triggers an osmotic stress response and chronic p38MAPK activation to promote long-term cell cycle arrest

Project description:<p>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 inhibitors that arrest cell cycle progression during G0/G1 and are used in the clinic to treat ER+/HER2- metastatic breast cancer. We demonstrate that CDK4/6 inhibition promotes cellular overgrowth during G0/G1, causing p38MAPK-p53-p21-dependent cell cycle withdrawal. We find that cell cycle withdrawal is triggered by two waves of p21 induction. First, overgrowth during a long-term G0/G1 arrest induces an osmotic stress response. This stress response produces the first wave of p21 induction. Second, when CDK4/6 inhibitors are removed, a fraction of cells escape long term G0/G1 arrest and enter S-phase where overgrowth-driven replication stress results in a second wave of p21 induction that causes cell cycle withdrawal from G2, or the subsequent G1. We propose a model whereby both waves of p21 induction contribute to promote permanent cell cycle arrest. This model could explain why cellular hypertrophy is associated with senescence and why CDK4/6 inhibitors have long-lasting effects in patients.</p>

2025-10-24 | MTBLS5868 | MetaboLights

Cell cycle arrest enhances CD8+ T cell effector function by potentiating glucose metabolism and IL-2 signaling

Project description:Cell cycle-inhibiting chemotherapeutics are widely used in cancer treatment. Although their primary aim is to block tumor cell proliferation, their clinical efficacy also involves specific effector CD8+ T cells that undergo synchronized proliferation and differentiation. How CD8+ T cells are programmed when these processes are uncoupled as occurs during cell cycle inhibition is unclear. Here, we demonstrate that activated CD8+ T cells arrested in their cell cycle can still undergo effector differentiation. Cell-cycle arrested CD8+ T cells become metabolically reprogrammed into a highly energized state, enabling rapid and enhanced proliferation upon release from arrest. This metabolic imprinting is driven by increased nutrient uptake, storage, and processing, leading to enhanced glycolysis in cell cycle-arrested cells. The nutrient sensible mTORC1 pathway, however, was not crucial. Instead, elevated IL-2 production during arrest activates STAT5 signaling, which supports expansion of the energized CD8+ T cells following arrest. Transient arrest in vivo enables superior CD8+ T cell-mediated tumor control across models of immune checkpoint blockade, adoptive cell transfer, and therapeutic vaccination. Thus, transient uncoupling of CD8+ T cell differentiation from cell cycle progression programs a favorable metabolic state that supports the efficacy of effector T cell-mediated immunotherapies.

2025-12-01 | GSE277143 | GEO

MicroRNA expression during cell cycle arrest

2011-09-15 | GSE31225 | GEO

Acetate Triggers Epigenetic Activation of Cell Cycle Arrest via ACSS2-H2A.Zac Axis in Esophageal Squamous Cell Carcinoma [ChIP-seq]

Project description:Acetate Triggers Epigenetic Activation of Cell Cycle Arrest via ACSS2-H2A.Zac Axis in Esophageal Squamous Cell Carcinoma [ChIP-seq]

| PRJNA1336786 | ENA

Acetate Triggers Epigenetic Activation of Cell Cycle Arrest via ACSS2-H2A.Zac Axis in Esophageal Squamous Cell Carcinoma [RNA-seq]

Project description:Acetate Triggers Epigenetic Activation of Cell Cycle Arrest via ACSS2-H2A.Zac Axis in Esophageal Squamous Cell Carcinoma [RNA-seq]

| PRJNA1336790 | ENA

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data