EGF (Epidermal growth factor)

The pathways affected are: Ephrin Receptor Signaling, TGF-β Signaling, STAT3 Pathway, EGF Signaling, Tumor Microenvironment Pathway, BAG2 Signaling Pathway, H-17A Signaling Pathway, EIF2 Signaling. Annexin-V and Tubulin tracker kits identified the apoptotic capabilities of the PR series compounds.

Interestingly, heparin did not enhance the proliferative activity of treated cells, likely because it binds to the heparin-binding domain of HB-EGF, sequestering it from interaction with membrane-associated heparan sulfate proteoglycans and preventing matricrine activation. These findings suggest that combining HB-EGF-targeting strategies could significantly reduce mitogenic activation and induce cancer cell death in tumors with high EGFR and proHB-EGF expression.

Conclusion Overexpression of GalNAc-T4 could significantly improve the mitochondrial dysfunction in H9c2 cells undergoing hypoxia/reoxygenation under high glucose conditions, inhibit oxidative stress and excessive mitochondrial autophagy, and reduce the apoptosis rate of cardiomyocytes. This may be related to its ability to block the activation of ERK1/2 signaling pathway.

IFX + AZA for rapid induction remission and RIF+AZA for maintenance therapy in IBD.

Our study establishes a robust EGF family gene-based prognostic model for CC patients and identifies AREG as a promising therapeutic target. These findings provide new insights for CC prognosis assessment and treatment strategies.

These results indicated that E2F8 promotes proliferation, migration, and invasion of EC cells by transcriptionally activating EGFL6.

We established a non-invasive 8-SPCG signature that may serve as a potential predictor for GC prognosis and TME features. SERPINE1 was identified as a promising mediator linking GC progression to CAFs interactions, supporting its further investigation as a therapeutic target.

Moreover, CD109 depletion promoted enhanced transforming growth factor-β1/Smad3 signaling and attenuated epidermal growth factor/AKT signaling in GBAC cells in a cell type-dependent manner. Collectively, these findings suggest that CD109 may serve as a prognostic biomarker of tumor progression and outcome in GBAC.

We emphasize opportunities to refine risk stratification, integrate hereditary cancer management, and adopt emerging tools, such as liquid biopsy, for early detection and disease monitoring. Ultimately, defining the biological foundations of YOGC may enable tailored interventions and improve prognosis in this increasingly relevant and understudied population.

Collectively, our study establishes miR-31 as a novel biomarker for LUAD proliferative potential and implicates the miR-31/CDK1-E2F2 network as a promising target for disrupting LUAD progression. These findings establish a miRNA-centric precision therapeutic paradigm for effectively suppressing oncogenic proliferation in LUAD.

Similarly, targeted inhibition of EGF partially reduced lung tumour growth in xenografts when senescent but not normal fibroblasts were co-implanted. Our findings have identified core SASP drivers of tumorigenesis and suggest that effective tumorigenesis driven by SASP is multifactorial and requires alterations in the target cells to achieve maximal response.

Furthermore, the addition of growth factors such as bFGF, EGF, or FGF significantly enhanced the formation of CSCs' spheroids. Most of the studies included in the review utilized a non-viral vector for the delivery of pluripotent gene markers into the cells.