ArticleClinical and translational medicine2025
Exosomal miR-3126-5p derived from cancer-associated fibroblasts facilitates glycolysis to accelerate NSCLC progression by targeting KLF13 to activate the SH2B1/IRS1 axis.
Article in Clinical and translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
- Clinical significance of miRNAs and exosomal miRNAs in non-small cell lung cancer: diagnostic, prognostic, and therapeutic perspectives.Journal of human genetics · 2026Review
- Exosomal miR-3126-5p derived from cancer-associated fibroblasts facilitates glycolysis to accelerate NSCLC progression by targeting KLF13 to activate the SH2B1/IRS1 axis.Clinical and translational medicine · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
backgroundAs a critical component of the tumour microenvironment, cancer-associated fibroblasts (CAFs) actively drive the malignant advancement of non-small-cell lung cancer (NSCLC); however, their underlying mechanisms continue to be poorly characterized. This work examined the role of CAFs-derived exosomal miR-3126-5p in the glycolysis of NSCLC cells.
methodsGlycolysis was evaluated by lactate production, glucose uptake, oxygen consumption rate (OCR) and extracellular acidification rate (ECAR). Cell proliferation and cycle were evaluated by CCK-8, EdU staining, and flow cytometry. Src homology 2B adaptor protein 1 (SH2B1) and insulin receptor substrate 1 (IRS1) protein interaction was tested by Co-IP and GST pull-down assay. ChIP, dual-luciferase reporter assay, and EMSA determined the binding of kruppel-like factor 13 (KLF13) to the SH2B1 promoter. Dual-luciferase reporter assay was applied to assess miR-3126-5p binding to KLF13 3'-UTR. In vivo growth of NSCLC was determined in the mouse xenograft and Lewis lung carcinoma models.
resultsCAFs-derived exosomal miR-3126-5p was highly expressed in NSCLC tissues, and its elevated plasma level was significantly associated with poor prognosis of NSCLC patients. CAFs-derived exosomal miR-3126-5p facilitated glycolysis to accelerate the malignant progression of NSCLC cells. KLF13 exhibited reduced expression in NSCLC, while its overexpression suppressed NSCLC growth via repressing glycolysis. Exosomal miR-3126-5p targeted KLF13 3'-UTR to inhibit its expression in NSCLC cells. KLF13 transcriptionally inhibited SH2B1 expression to abolish the interaction between SH2B1 and IRS1 proteins, thus repressing PI3K/AKT pathway-mediated glycolysis. KLF13 knockdown counteracted the anti-cancer action of exosomal miR-3126-5p inhibition.
conclusionCAFs-derived exosomal miR-3126-5p accelerated NSCLC progression via inhibiting KLF13 expression, which transcriptionally activated SH2B1 to promote its interaction with IRS1, thereby promoting PI3K/AKT pathway-mediated glycolysis. Our findings position CAFs-secreted exosomal miR-3126-5p as a novel therapeutic intervention with potential in NSCLC management. HIGHLIGHTS: CAFs-derived exosomal miR-3126-5p enhanced glycolysis of NSCLC cells via targeting KLF13. KLF13 led to transcriptional inhibition of SH2B1 in NSCLC cells. SH2B1 interplayed with IRS1 to facilitate glycolysis of NSCLC cells. IRS1 promoted glycolysis of NSCLC cells via the activation of PI3K/AKT pathway.
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.