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Record W4407588098 · doi:10.1016/j.jhepr.2025.101354

Salsalate improves the anti-tumor efficacy of lenvatinib in MASH-driven hepatocellular carcinoma

2025· article· en· W4407588098 on OpenAlexafffund
Evangelia E. Tsakiridis, Elham Ahmadi, Jaya Gautam, Yun She, Russta Fayyazi, James Lally, Simon Wang, Fiorella Di Pastena, Celina M Valvano, Olga‐Demetra Biziotis, Brandon M. Meyers, Paola Muti, Theodoros Tsakiridis, Gregory R. Steinberg

Bibliographic record

VenueJHEP Reports · 2025
Typearticle
Languageen
FieldBiochemistry, Genetics and Molecular Biology
TopicCancer, Lipids, and Metabolism
Canadian institutionsJuravinski Cancer CentreMcMaster UniversityMcMaster University Medical Centre
FundersMcMaster UniversityCanadian Institutes of Health ResearchHamilton Health Sciences
KeywordsLenvatinibHepatocellular carcinomaMedicineOncologyInternal medicineCarcinomaSorafenib

Abstract

fetched live from OpenAlex

Background & Aims Metabolic dysfunction-associated steatohepatitis (MASH) is a growing cause of hepatocellular carcinoma (HCC) worldwide. The complex microenvironment of these tumors, characterized by metabolic dysfunction, hypoxia, steatosis, and fibrosis, limits the effectiveness of standard-of-care therapies, such as the multi-tyrosine kinase inhibitor lenvatinib (LEN). Salsalate (SAL), is a rheumatoid arthritis therapy that enhances fatty acid oxidation and reduces de novo lipogenesis, fibrosis and cell proliferation pathways. We hypothesize that addition of SAL could improve the efficacy of LEN in MASH-HCC. Methods We assessed the efficacy of combination therapy using clinically relevant concentrations of LEN and SAL in human HCC cell models, orthotopic xenograft and MASH-HCC mouse models. In addition, assays assessing fatty acid oxidation and lipogenesis, protein immunoblotting and RNA-sequencing were used to understand mechanisms involved. Results LEN + SAL synergistically suppressed the proliferation and clonogenic survival of cells ( p ≤0.0001), prolonged survival in an orthotopic xenograft model ( p = 0.02), and reduced angiogenesis, fibrosis, and steatosis ( p ≤0.05) in a MASH-HCC model. These effects were associated with activation of AMPK and inhibition of the mTOR-HIF1α and Erk1/2 signaling pathways. RNA-sequencing analysis in both Hep3B cells and livers of the MASH-HCC mouse model revealed that SAL enhanced fatty acid oxidation and suppressed fibrosis and cell cycle progression, while LEN reduced angiogenesis with regulatory network analysis, suggesting a potential role for activating transcription factor 3 (ATF3) and ETS-proto-oncogene-1 (ETS-1). Conclusions These data indicate that combining LEN and SAL, which exert distinct effects leading to improvements in the liver microenvironment (steatosis, angiogenesis, and fibrosis) and inhibition of tumor proliferation, may have therapeutic potential for MASH-driven HCC. Impact and implications Although rates of MASH-HCC are on the rise globally, standard-of-care multi-tyrosine kinase inhibitors and immunotherapy have limited efficacy in this HCC etiology. Metabolic targeting with SAL inhibits cancer growth kinetics while also alleviating drivers of MASH by increasing fatty acid oxidation and reducing de novo lipogenesis and fibrosis. Combined LEN and SAL improved survival and MASH-HCC pathology in mouse models without adverse effects. Given that SAL is a safe, economical, and approved medication, this concept holds great translational potential that could provide a new treatment avenue for patients with unresected MASH-HCC.

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 distilled prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. Learned from the 10,348 direct Codex labels and 10,348 direct Gemma labels. Candidate is the union of thresholded teacher heads; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels or direct frontier model labels.

metaresearch head score (Codex)0.000
metaresearch head score (Gemma)0.000
Version: codex-gemma-dda1882f352aValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Bench or experimental · Consensus signal: none
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.541
Threshold uncertainty score0.473

Codex and Gemma teacher scores by category

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

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 head0.007
GPT teacher head0.242
Teacher spread0.235 · 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 teacher head, 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 routes2
Has abstractyes

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