ArticleScientific reports2026
The KRT15 and KRT81 complex promotes lenvatinib resistance in thyroid cancer by upregulating DGKB mediated lipid metabolism.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lenvatinib resistance is a major clinical obstacle in the treatment of radioiodine-refractory papillary thyroid cancer (PTC). Clarification of the molecular mechanisms of this resistance is of utmost importance to devise effective therapeutic strategies. We investigated the role of Keratin 15 (KRT15) in lenvatinib resistance through comprehensive in vitro and in vivo studies. Tumor and normal thyroid tissues were analyzed for KRT15 expression and correlation with patient survival. Metabolic profiling was performed to investigate KRT15-dependent alterations in lipid metabolism, namely fatty acid oxidation (FAO). Mechanistic investigations explored the interaction between KRT15, Keratin 81 (KRT81), and Diacylglycerol Kinase B (DGKB). The therapeutic potential of targeting this pathway was evaluated using shRNA-mediated knockdown and pharmacological inhibition. KRT15 overexpression was associated with unfavorable clinical prognosis in thyroid cancer patients. We identified that KRT15 interacts with KRT81 to constitute a regulatory complex, which induces DGKB upregulation. The KRT15-KRT81-DGKB axis controls metabolic reprogramming by upregulating key FAO enzymes (CPT1A and ACOX1), resulting in increased cellular energetics and survival against therapeutic stress. Inhibition of this pathway successfully restored lenvatinib sensitivity in resistant cells. This study illustrates a novel mechanism of cytoskeletal proteins involvement in metabolic adaptation of drug-resistant thyroid cancer cells. The KRT15-KRT81-DGKB pathway is a promising therapeutic target, particularly in combination with lenvatinib, for refractory thyroid cancer patients.
Indexed as
Identifiers
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.