Copyright: ©Author(s) 2026.
World J Gastroenterol. Jun 7, 2026; 32(21): 116467
Published online Jun 7, 2026. doi: 10.3748/wjg.v32.i21.116467
Published online Jun 7, 2026. doi: 10.3748/wjg.v32.i21.116467
Table 1 Key contributions of the study on IGF2BP3/FBXO32/cyclic guanosine monophosphate-protein kinase G axis in gastric cancer
| Contribution category | Core content | Innovation & significance |
| Mechanistic elucidation | First reveals IGF2BP3 promotes GC via m6A-dependent regulation: Binds FBXO32 mRNA to upregulate its protein (no transcriptional change) | Fills IGF2BP3 downstream gap in GC; unique mechanism; identifies FBXO32 as key m6A effector |
| Axis identification | Identifies IGF2BP3/FBXO32/cGMP-PKG as GC driver; KT5823 (PKG inhibitor) reverses its oncogenic effects | Links cGMP-PKG to IGF2BP3/FBXO32 (novel in GC); validates druggable target |
| Translational relevance | High IGF2BP3 = poor prognosis (prognostic biomarker); axis targeting offers new therapy | Bridges preclinical-clinical translation; aids prognosis/treatment |
- Citation: Xu S, Zhu Z, Shi PH, Xu YT, Zhang HM, Zheng Y, Chen YT, Lu GR, Zheng BJ. Letter to the Editor: Targeting the IGF2BP3/FBXO32/cGMP-PKG axis as a therapeutic modality for gastric cancer: A promising strategy. World J Gastroenterol 2026; 32(21): 116467
- URL: https://www.wjgnet.com/1007-9327/full/v32/i21/116467.htm
- DOI: https://dx.doi.org/10.3748/wjg.v32.i21.116467