ArticleOncotarget2025
The SCD1 inhibitor aramchol interacts with regorafenib to kill GI tumor cells
Article in Oncotarget, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Synergistic mechanisms and clinical translation of regorafenib combination therapies.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- Targeting the lipid desaturation network in cancer: from metabolic plasticity to precision therapeutics.Journal of experimental & clinical cancer research : CR · 2026Review
- The SCD1 inhibitor aramchol interacts with regorafenib and metformin to kill tumor cells.Oncotarget · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
The anti-tumor actions of the Stearoyl-CoA desaturase (SCD1) inhibitor aramchol in tumor cells remains poorly understood. Aramchol interacted with the multi-kinase inhibitors sorafenib, regorafenib or lenvatinib, to kill GI tumor cells, with regorafenib exhibiting the greatest effect. In HCT116 cells homozygous for the autophagy-regulatory protein ATG16L1 T300, aramchol and regorafenib interacted to activate ATM and the AMPK and to inactivate mTORC1 and mTORC2. As a single agent, regorafenib inactivated eIF2α and it combined with aramchol to elevate GRP78 expression. In HCT116 cells expressing the ATG16L1 A300 isoform the drug-induced dephosphorylation of mTORC1 S2448 and mTORC2 S2481 and the increased phosphorylation of eIF2α S51 were significantly lower than in T300 cells. In cells expressing ATG16L1 T300, but not A300, regorafenib and/or the drug combination inactivated AKT, ERK1/2 and p70 S6K. Regorafenib and aramchol interacted to cause formation of autophagosomes which was significantly greater in cells expressing ATG16L1 T300. Aramchol as a single agent did not stimulate autophagic flux but further enhanced both flux and autolysosome formation caused by regorafenib. Knock down of Beclin1 reduced the lethality of regorafenib and aramchol as single agents and when combined whereas knock down of LAMP2 or BID did not reduce killing caused by aramchol as a single agent but did reduce the lethality of regorafenib alone and regorafenib plus aramchol.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.