CREB3L1 (CAMP Responsive Element Binding Protein 3 Like 1)

Acting as a glycan rheostat, GNASR201C elevates LacdiNAcs at the expense of pro-tumorigenic acidic Lewis epitopes, inhibiting cancer cell invasion and disease progression. LacdiNAcs and 3'-sulfo-LeA/C are mutually exclusive and may serve as markers to risk stratify IPMN patients for surgery.

Subsequently, the pro-cancerous effects of GTs were validated through a series of experiments, including CCK-8 cell viability assays, scratch wound healing assays, and Transwell migration and invasion assays. This research lays the foundation for targeted drug therapies, offering new opportunities to enhance clinical outcomes in TNBC.

In GH3 xenograft nude mice, administration of deguelin (4 mg/kg, i.p., every other day for two weeks) significantly inhibited tumor growth with significant reduction in both AKT phosphorylation and CREB3L1 levels in deguelin-treated xenografts. These results suggest that deguelin can be considered a therapeutic option for treating DA-resistant prolactinoma and serve as a basis for developing novel treatment approaches.

Ultra-rare GMN-TDGAs included a PTCH1::GLI1-positive renal epithelioid mesenchymal neoplasm, a BRAF-deleted renal spindle cell tumor, and a MYOD1-mutated prostatic spindle cell rhabdomyosarcoma. Conclusively, molecular profiling highlights the histologic and genetic diversity of GMNs, supporting challenging diagnoses and informing personalized therapies.

In this work, we identified a set of candidate TFs with the potential to induce a cell state transition favoring a switch from nonhealing to healing outcomes in patients with nonhealing DFU. Overall, our gene regulatory network-driven TF cocktail provides a rational blueprint for reprogramming DFU cell states and paves the way toward targeted regenerative therapies.

Molecularly targeted therapies constitute the cornerstone of current strategies, with vemurafenib inhibiting BRAF/MEK in PTC, sorafenib acting as a multikinase suppressor in FTC, vandetanib blocking RET in MTC and berberine-doxorubicin combinations overcoming chemoresistance in ATC. Metabolic interventions, including metformin for glucose modulation in PTC and novel delivery systems such as micelle-encapsulated AB3 for MTC, demonstrate translational potential. The present review summarizes molecular mechanisms, diagnostic tools and emerging therapies while emphasizing the necessity of subtype-specific approaches to improve clinical outcomes in thyroid oncology.

This study revealed the heterogeneity of fibroblasts in DF for the first time. The novel gene markers and transcription factor identified in DF and the significance of neural cells in the tumor microenvironment may point to new directions for the targeted therapy of DF in the future.

Interestingly, treatment with rosuvastatin also led to a significant reduction in viral replication, but only when administered before infection. The present study is the first demonstration of a Golgi response to YFV infection and highlights a mechanism that could be targeted by future antiviral therapeutic strategies.

Our results suggest that HGSC can be classified based on lncRNA expression and characterized using molecular features. Therefore, lncRNAs and MTFs may synergistically contribute to molecular features of HGSC that could be indicators for personalized medicine.

No patients had a known history of familial adenomatous polyposis. We describe a novel fibroblastic soft tissue neoplasm characterized by co-expression of MUC4 and beta-catenin and frequent underlying APC inactivation, for which we propose the name "MUC4-positive fibroblastoma."

ROR1 knockdown resulted in the re-expression of CREB3L1 in TNBC cells. The data provide evidence that ROR1 inhibition, in combination with DNMTis, could enhance patient outcomes as a therapeutic approach for TNBC.

Finally, in a mouse metastasis assay, expression of CREB3L1 in NCI-H2170 cells significantly reduced the formation of liver metastases and in NCI-H226 cells, lung metastases, as compared to their respective CREB3L1-deficient parental LUSC cells. Taken together, these results strongly support a role for CREB3L1 as a metastasis suppressor in lung squamous cell carcinoma cells.