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Record W4414830180 · doi:10.1113/jp288099

Breast cancer cell‐conditioned media inhibit growth and reduce basal and insulin‐stimulated glucose uptake by inhibiting Rac1 activation in rat myotubes

2025· article· en· W4414830180 on OpenAlexfundno aff
Mona Sadek Ali, Stine Bitsch‐Olsen, Emma Frank, Scott Sebastian Birch Themsen, Edmund Battey, Mirela Perla, Steffen H. Raun, Steven de Jong, Lykke Sylow

Bibliographic record

VenueThe Journal of Physiology · 2025
Typearticle
Languageen
FieldBiochemistry, Genetics and Molecular Biology
TopicMetabolism, Diabetes, and Cancer
Canadian institutionsnot available
FundersDanmarks Frie ForskningsfondNovo Nordisk FondenDanmarks GrundforskningsfondHospital for Sick ChildrenDanish Diabetes AcademyNational Research FoundationNovo Nordisk
KeywordsGLUT4Glucose uptakeMyogenesisSkeletal muscleBreast cancerRAC1Glucose transporterBasal (medicine)

Abstract

fetched live from OpenAlex

Abstract Metabolic disorders are common in women with breast cancer, raising mortality and recurrence rates, but their causes remain poorly understood. Given the importance of skeletal muscle metabolism in glucose homeostasis, we investigated the effect of breast cancer cell‐conditioned media on insulin‐stimulated glucose uptake in muscle. Rat L6 myotubes overexpressing myc‐tagged GLUT4 were incubated with 40% conditioned media from tumourigenic MCF7 or BT474, or non‐tumourigenic control MCF10A breast cells. Mass‐spectrometry‐based proteomics was applied to detect molecular rewiring in response to breast cancer in the muscle. Expression of myogenesis and inflammation markers, GLUT4 translocation, [ 3 H]2‐deoxyglucose uptake, and intramyocellular insulin signalling were determined. Breast cancer cell‐conditioned media induced proteomic changes in pathways linked to sarcomere organisation, actin filament binding and vesicle trafficking. Myogenic differentiation was disrupted, marked by a 50% increase in Mki67 mRNA and trend ( P = 0.087) towards reduced myosin heavy chain expression, as shown by immunofluorescence. Additionally, breast cancer cell‐conditioned media activated inflammation via nuclear factor‐κB and interleukin‐6 signalling and reduced myotube width by 70% ( P = 0.0524). Myotubes treated with breast cancer cell‐conditioned media had a reduced basal and insulin‐stimulated GLUT4 translocation and glucose uptake. Insulin signalling via the Rho GTPase Rac1 was reduced by 40%, while absolute Akt–TBC1D4 phosphorylation was unaffected. Conditioned media from MCF7 and BT474 breast cancer cells altered skeletal muscle proteome, induced inflammation, lowered growth markers, reduced glucose uptake, inhibited GLUT4 translocation and blocked insulin‐stimulated Rac1 activation. These findings indicate that the rewiring of skeletal muscle could play a role in metabolic dysfunction in patients with breast cancer. image Key points Metabolic disorders in breast cancer increase mortality and cancer recurrence. Here, we show that incubation with breast cancer cell‐conditioned media (CM) alters the proteome in rat skeletal muscle cells. In addition, breast cancer CM activates NF‐κB and type 1 interferon pathways, inhibiting muscle growth. Moreover, breast cancer CM inhibits basal and insulin‐mediated GLUT4 translocation and glucose uptake, likely by blocking insulin‐stimulated Rac1, but not Akt–TBC1D4 activation. These results underscore a potential mechanistic link between breast cancer and metabolic disorders and suggest that skeletal muscle rewiring may play a role.

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

How this classification was reachedexpand

Full frame machine prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.

metaresearch head score (Codex)0.000
metaresearch head score (Gemma)0.000
Version: metacan-v3-hybrid-931329e0061cValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Bench or experimental · Consensus signal: Bench or experimental
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.003
Threshold uncertainty score0.008

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0000.000
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0000.001
Bibliometrics0.0000.000
Science and technology studies0.0000.000
Scholarly communication0.0000.000
Open science0.0000.000
Research integrity0.0000.001
Insufficient payload (model declined to judge)0.0030.001

Machine scores (provisional)

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

Opus teacher head0.005
GPT teacher head0.237
Teacher spread0.231 · how far apart the two teachers sit on this one work
Validation statusscore_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Classification

machine, unvalidated

Machine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.

The models applied no category: nothing in the taxonomy fit this work.
Study designBench or experimental
Domainnot available
GenreEmpirical

How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".

Quick stats

Citations0
Published2025
Admission routes1
Has abstractyes

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