SRF (Serum Response Factor)

SRF overexpression in glioblastoma is associated with increased angiogenesis and higher recurrence risk. SRF may promote tumour proliferation, differentiation, and migration, and serve as a prognostic biomarker and potential therapeutic target.

SRF is overexpressed in glioblastoma and closely linked to tumor angiogenesis and postoperative recurrence. High SRF expression may promote tumor progression through vascular remodeling, suggesting its potential utility as a prognostic biomarker and therapeutic target in GBM management.

SRF is highly expressed in high-grade glioma and is positively correlated with MVD. It is closely associated with postoperative recurrence and may serve as a potential biomarker for glioma progression and recurrence prediction.

A smaller subset with more worrisome morphologic features harbor biallelic inactivation of TP53. To emphasize their unique features, we propose the term "pediatric-type myoid neoplasms of somatic soft tissue," rather than simply "leiomyoma" or "leiomyosarcoma" for group 1 tumors and the designation of leiomyosarcoma in children should be limited to group 2 tumors.

Multiplexed quantitative immunohistochemistry and transcriptome analyses of clinical BC specimens further demonstrate a positive correlation between nuclear localization of MRTF with malignant traits of cancer cells and enrichment of MRTF-SRF gene signature in pair-matched distant metastases vs primary tumors. In conclusion, this study establishes a novel mechanism of MRTF-dependent regulation of cell migration and provides evidence for the association between MRTF activity and increased malignancy in human breast cancer, justifying future development of specific small molecule inhibitors of the MRTF-SRF transcriptional complex as potential therapeutic agents in breast cancer.

Changes in endothelial cells involve increased expression of serum response factor target genes, and, strikingly, major aspects of the LATS2 mutant phenotype are rescued by inactivation of the Srf gene. These findings identify the endothelium as a driver of bone marrow fibrosis, which improves understanding of myelofibrotic and osteosclerotic diseases, for which drug therapies are currently lacking.

TRIM28 is crucial in the development of GC, and may regulate IDO1 through SRF. TRIM28 promote GC cell proliferation through SRF/IDO1 axis.

Our findings dissect the cellular roles of YAP, TAZ, and SRF in prostate cancer cells. Our data emphasize the interplay between these transcriptional regulators and their roles in prostate tumorigenesis and highlight how these insights might be exploited therapeutically.

We revealed a novel molecular mechanism through which SRF modulates OSCC metastasis. This should provide potential targets or biomarkers for OSCC diagnosis and treatment.

We highlight key clinical, pathological, and molecular features. As we illustrate, these rare tumors pose a considerable diagnostic challenge, and risk misdiagnosis as sarcoma, most notably spindle cell rhabdomyosarcoma.

We screened for potential SRF activators in CSF and found that fibroblast growth factor 17 (Fgf17) infusion is sufficient to induce OPC proliferation and long-term memory consolidation in aged mice while Fgf17 blockade impairs cognition in young mice. These findings demonstrate the rejuvenating power of young CSF and identify Fgf17 as a key target to restore oligodendrocyte function in the ageing brain.