FYN (FYN Proto-Oncogene, Src Family Tyrosine Kinase)

IQGAP3 drives immunosuppressive macrophage polarization in LUAD. Its inhibition represents a novel strategy to improve immunotherapy response.

Although interventions such as electroacupuncture can exert neuroprotective effects by activating FTO, clinical translation still faces challenges such as insufficient targeting specificity and difficulty in penetrating the blood-brain barrier. In the future, it is necessary to combine single-cell multi-omics and spatiotemporal dynamic analysis to analyze the FTO regulatory network, and develop a cell-selective delivery system to promote the development of novel neuroprotective strategies targeting the FTO-m6A axis.

Exosomes derived from sh-FYN glioma cells weakened macrophage M2 polarization and reduced CXCL1, IL-10 and TGF-β secretion, revealing an immunometabolism axis. Collectively, these results establish FYN as the mechanistic conduit between glyphosate and GBM and demonstrate that targeting FYN-directly or via exosome delivery-reprograms tumor glycolysis and immunity, offering a tractable strategy against glyphosate-associated malignancy.

Hepatitis B virus (HBV) integrates in both tumour and adjacent para-tumour tissues of pancreatic ductal adenocarcinoma (PDAC). KMT2B, a target gene of HBV integration, promotes PDAC proliferation and metastasis in vivo and in vitro experiments. KMT2B exerts its oncogenic effects by regulating the downstream target gene FYN via histone H3K4 trimethylation, activating the PI3K/Akt signalling pathway.

Our findings identify FYN, LGALS8, MAGI2, and WT1 as hub genes in KIRC, with potential diagnostic and prognostic value. These genes play significant roles in methylation, mutation, and immune regulation in KIRC. However, the results from the limited MN samples suggest possible roles of these genes in MN pathology, but further studies are required to fully assess the relevance of these findings to MN.

RNF144B and FYN expression exhibit opposing trends in peripheral blood across BM stages, suggesting their potential as biomarkers for diagnosis and monitoring. These findings provide a valuable reference for early intervention strategies and personalized treatment approaches tailored to specific disease stages in the clinic.

Our findings reveal that NMN promotes FGSC proliferation by activating the H4K16ac-Hmgb1-Fyn-PLD signaling pathway through epigenetic remodeling. These results deepen our understanding of FGSC proliferation and highlight potential therapeutic avenues for advancing FGSC applications in reproductive medicine.

By employing pairwise tyrosine kinase knockout CRISPR screens, we identify FYN and KDM4 as critical targets whose inhibition enhances the effectiveness of TKIs, such as NVP-ADW742 (IGF-1R inhibitor), gefitinib (EGFR inhibitor), and imatinib (ABL inhibitor) both in vitro and in vivo. FYN expression is associated with therapy resistance and persistence by demonstrating its upregulation in various experimental models of drug-tolerant persisters and residual disease following targeted therapy, chemotherapy, and radiotherapy. Collectively, our study provides novel targets and mechanistic insights that can guide the development of effective combinatorial targeted therapies, thus maximizing the therapeutic benefits of TKIs.

Moreover, paclitaxel-derived PDTPs show increased sensitivity to EGFR TKI Gefitinib and its combination with paclitaxel selectively induced cell death in Paclitaxel-derived PDTP (PDTP-P) TNBC cells and 3D spheroids by strongly downregulating phosphorylation of EGFR-Src with concomitant downregulation of Lyn and Fyn tyrosine kinases. Collectively, this study identifies a unique hyper-phosphorylation cellular state of TNBC PDTPs established by switching of EGFR-Src family tyrosine kinases, creating a vulnerability to EGFR TKI.

USP8-dependent FYN contributed to the malignant progression of ESCC by interacting with PTK2. Targeting this pathway may offer a novel therapeutic strategy for ESCC treatment.

We describe our patient's clinical course, differential diagnosis, and potential implications of FYN deletion on disease pathogenesis. To our knowledge, this is the first report of an FYN structural alteration to be described in PCGDTCL.

Enriched gene ontology terms included "Signaling by Rho GTPases," "Signaling by receptor tyrosine kinases," and "immune system." Additionally, nine hub genes-FYN, MAPK3, CDK2, SNRPG, GNAQ, PAK1, LPCAT4, MAP1LC3B, and FBN1-were identified as central to PDAC pathogenesis. This integrated approach, combining co-expression analysis with protein-protein interaction network analysis using a metaheuristic algorithm, provides valuable insights into PDAC mechanisms and highlights several hub genes as potential therapeutic targets.