SOX18 (SRY-Box Transcription Factor 18)

Regulation of SOX18 by miR-24-3p highlights a potential therapeutic vulnerability. These findings underscore the significance of SOX transcription factors as biomarkers and potential targets for novel treatment strategies in NSCLC.

In contrast, GC cells in the miR-1343-3p inhibitor group showed decreased expression of miR-1343-3p and increased expression of SOX18 mRNA and protein (all P < 0.05). Salidroside may inhibit the proliferation of GC cells by regulating the miR-1343-3p/SOX18 signaling axis and these regulators may present new potential therapeutic targets or biomarkers for gastric cancer.

Protein-protein interaction (PPI) network analysis showed that the effect of MEF2C on OS may be related to genes such as APOE and SOX18. The results of this study suggest that MEF2C is associated with an increased risk of OS and that MEF2C has the potential to be a prognostic biomarker for OS.

Disruption of SOX18 or BRG1-genetically or pharmacologically-leads to reduced episome load and attenuated hallmarks of virus infection. This work highlights how viruses can harness lineage-specific transcriptional regulators to establish persistent nuclear retention of their episome into the host genome.

Using CRISPR-Cas9-mediated enhancer interference and SNP editing, we demonstrated that glioma-specific enhancer carrying the risk SNP rs2297440 regulates SOX18 expression by specifically recruiting transcription factor MEIS1 binding, thereby contributing to glioma progression. Our study sheds light on the molecular mechanisms underlying glioma susceptibility and provides potential therapeutic targets to treat glioma.

Histopathologically, this phenomenon is manifested through lymphangiogenic mimicry, which can be classified into lymphatic-like, mosaic, and lymphatic types. This study presented a theoretical framework to elucidate the developmental mechanisms driving cancer cell lymphatic endothelialization and provided a new theoretical basis for understanding the cellular origin of tumor-associated neolymphatic vasculature and introduces new pathways for investigating mechanisms of tumor lymphangiogenesis and metastasis, thereby providing potential avenues for clinical treatment strategies.

Disruption of SOX18 or BRG1-genetically or pharmacologically-leads to reduced episome load and attenuated hallmarks of virus infection. This work highlights how viruses can harness lineage-specific transcriptional regulators to establish persistent nuclear retention of their episome into the host genome.

Pan-cancer analysis revealed that MMP11+ mCAFs are present across various cancer types, including breast cancer, lung adenocarcinoma, gastric cancer, and colorectal cancer. These findings provide insights into the heterogeneity of CAFs and their regulatory role in tumor progression, offering new potential therapeutic targets for CAF-targeted treatments with broad applicability across cancers.

This study revealed the clinical relevance of histone H4R3me2a modification in HCC and demonstrated that PRMT1 promotes malignant behavior in HCC cells by modulating H4R3me2a modification in the SOX18 promoter region. The findings elucidate the role and molecular mechanism of PRMT1-mediated histone H4R3me2a modification in HCC progression and highlight the potential clinical applications of PRMT1 inhibitors. These results may provide new insights into the treatment of HCC.

SOX18 plays a critical role in NPC progression by affecting key cellular behaviors. Targeting SOX18 may offer new therapeutic strategies and improve prognostic assessments for NPC patients, highlighting its potential as a valuable molecular marker for cancer treatment.

We propose an novel endothelial SOX18-MVP-axis as a central regulator of IH pathogenesis and suggest statin repurposing to treat IH. The pleiotropic effects of R(+) propranolol and statins along the SOX18-MVP axis to disable an endothelial-specific program may have therapeutic implications for other vascular disease entities involving pathological vasculogenesis and angiogenesis.

The SOX gene family is closely implicated in the onset and progression of lung adenocarcinoma, of which most members may be used as prognostic marker genes for patients.