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. 2026 Jul 11;45:185. doi: 10.1186/s13046-026-03748-w

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© The Author(s) 2026

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 4 — β-catenin/c-Myc axis mediates S100A9-driven fatty acid metabolic reprogramming in EGFR-wild-type tumor cells. A β-catenin silencing attenuated intracellular FFA levels induced by mtLC-MSCs. B, C β-catenin silencing reduced transcriptional (B) and protein (C) levels of c-Myc and downstream targets. D c-Myc silencing diminished intracellular FFA levels by mtLC-MSCs. E, F c-Myc silencing decreased the transcriptional (E) and protein (F) expression of downstream targets. G c-Myc or β-catenin silencing, alone or in combination, decreased FASN and GULT1 protein expression. H-I β-catenin translocated to cytoplasmic and nucleus (H), while c-Myc accumulated in nucleus (I) upon mtLC-MSCs-conditioned medium treatment. J, K ChIP-qPCR identified c-Myc binding sites in the promoter of downstream genes in A549 (J) and H1385 (K) cells exposed to mtLC-MSCs-conditioned medium. L FASN silencing reduced intracellular FFA levels upregulated by mtLC-MSCs. M, N Knockdown c-Myc concurrently overexpress β-catenin increased GLUT1, but decreased FASN expression. O Stem-trait protein levels under conditioned medium treatment. P, Q FASN silencing reduced the upregulated transcriptional (P) and protein (Q) levels of stem-trait proteins induced by mtLC-MSCs. NANOG and CD44 transcriptional levels were too low to be detected in H1385 cells (P). Consistent treatment as above described. Statistical results were shown as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001, **** P < 0.0001. One-way ANOVA test except panel I (Student’s t-test). FFA, free fatty acid; GLUT1, glucose transporters 1; FASN, fatty acid synthase; ACACA, Acetyl-CoA carboxylase alpha; ACACB, Acetyl-CoA carboxylase beta; ACLY, ATP citrate lyase