FGF7 (Fibroblast Growth Factor 7)

Conclusions Our study revealed novel intercellular communication signatures involving aPSCs in T1D. Identification of the changes in cellular communication between aPSCs and other cells in T1D suggest a role in T1D pathogenesis or progression which might lead to the development of novel therapeutics.

The results of this study may help develop an effective treatment for EGFR-TKI-mediated rashes. The findings will be published in academic journals upon the completion of the trial.

All nanochitin could regulate Vascular Endothelial Growth Factor (VEGF) and Fibroblast Growth Factor-7 (FGF-7) secretion, potentially promoting angiogenesis and dermal repair-related biological processes, with hydrochloric acid hydrolyzed nanochitin (HNCh) having the strongest pro-secretory effect, increasing VEGF levels by 30.0%. Moreover, all four types of nanochitin effectively promote hair growth in mice; DNCh and phosphoric acid hydrolyzed nanochitin (PNCh) groups demonstrated superior therapeutic outcomes, with earlier emergence of dense hair shafts compared to HNCh and amphoteric nanochitin (ANCh) groups, while ANCh demonstrated the most balanced and optimal overall effect.

In the tumor microenvironment of breast cancer, intercellular communication pairs of different cell types and molecules can exacerbate the development of breast cancer. among them, through the present study, we found that CXCL12-CXCR4 and FGF7-FGFR1 are the most important. Also, most significantly differentially expressed genes including CHRDL1, SCARA5, LYVE1, PI16, and SAA2 seemed to play a critical role in these mechanisms and immune cell infiltration, shaping the TME of BC.

Further analysis indicated hsa-mir-221-3p and hsa-mir-29a-3p as key miRNAs targeting LBBC-related genes. Collectively, our findings highlighted LBBC-associated genes, TFs, miRNAs, and pathways as prospective biomarkers, providing insights into LBBC diagnosis and therapeutic approaches.

Knockdown of Angptl4 or Prl8a6 in periwound skin tissue impairs EpSC proliferation and delays wound re-epithelialization. In conclusion, our study demonstrates that, after skin injury, elevated levels of proinflammatory cytokines and growth factors in periwound tissue stimulate Angptl4 expression in EpSCs and that ANGPTL4 promotes EpSC proliferation by increasing Prl8a6 expression, thereby accelerating wound re-epithelialization.

Protein interaction analysis highlighted key hubs linking MAPK, SMAD, and dopamine signaling. This study elucidates crucial molecular intersections between MAPK, SMAD, and dopamine pathways, identifying potential biomarkers and therapeutic targets for breast cancer.

Our results also report the strong decreased expression of ERRγ and GPER (two receptors that bind estrogen or xenoestrogens) in diffuse and intestinal subtypes. Our study identified new target genes, namely hormone receptors and membrane receptors (ERRγ and GPER), whose expression is associated with an aggressive phenotype of diffuse GC, and revealed the importance of epigenetic factors (EZH2, HOTAIR, H19 and DNMT1) in gastric cancers.

Our study results indicate that only specific types of FGFs and FGFRs may have a causal relationship with BC. Th research provides a new perspective on the mechanisms of action of different types of FGFs and FGFRs in BC, and offers potential genetic support for personalized medicine and precision therapy.

Hypoxia-induced exosomal METTL14 supports the proliferation, metastasis, and glycolysis of TNBC cells through regulating TRIM16-mediated FGF7 ubiquitination, providing a promising therapeutic target for TNBC treatment.

Primary ovarian leiomyosarcomas exhibit a complex genomic landscape marked by genomic instability, sharing key alterations with uterine leiomyosarcomas. TP53 and PTEN mutations may play a central role in their pathogenesis. This first genomic profiling analysis of ovarian leiomyosarcomas provides a basis for further research and potential targeted therapeutic approaches in this rare malignancy.

Together, our analysis maps potential nociceptive signaling pathways of different MM microenvironment cell types. These pathways extend from upstream regulatory kinases to transcription factors to secreted ligands, which can potentially stimulate sensory neuron receptors in the bone.