FOXD3 (Forkhead Box D3)

Here, we show that the oligodendrocyte markers olig1 and plp1b are not expressed in MEP glia. These findings refine the molecular signature of MEP glia, enhancing their peripheral identity.

Furthermore, SENCR upregulates FOXD3 mRNA, an effect also abolished by miR-3648. In conclusion, the rs12420823 C allele confers protection against TNBC, and lncRNA SENCR acts as a tumor suppressor by sponging miR-3648 to regulate FOXD3, underscoring its prognostic and therapeutic relevance.

FOXD3-AS1 influences PCa cell behavior via the miR-491-5p/PEG10 axis.

Our study provides novel clinical and genetic evidence that family history of hypertension is significantly associated with thyroid cancer in women. Integrating hypertension-related screening with genetic profiling may enhance risk stratification and aid in the development of personalized management strategies to reduce overtreatment.

VISTA overexpression and FOXD3 downregulation in B-ALL, alongside altered CD48, and PVRL2 expression, highlight mechanisms of immune evasion. These findings position VISTA as a promising biomarker and target for B-ALL immunotherapy.

Inhibition of FOXD3 expression compromises HR-mediated DSB repair and chromosome stability and sensitizes cancer cells to ionizing radiation. Collectively, our findings demonstrate that FOXD3 promotes HR-mediated DSB repair and genome stability.

We identified a novel risk signature consisting of four PRlncRNAs, which is an independent prognostic indicator for patients with COAD. This PRlncRNA risk signature is potentially relevant for immunotherapy and could serve as a therapeutic target for COAD.

Kaplan-Meier curves and nomograms showed that FOXD1, FOXD3, and FOXD4 were prognostically significant. In conclusion, FOXD subfamily members (especially FOXD3) could serve as diagnostic and prognostic biomarkers for CRC and an immunotherapy target in patients with CRC.

In vivo experiments demonstrated that SLC5A6 knockout effectively inhibited tumor growth. These findings suggest that SLC5A6 is a potential therapeutic target for LUAD, offering a new avenue for treatment strategies.

The findings indicate that PTEN null BRAFV600E melanoma exhibits increased reliance on ERBB/HER signaling when treated with clinically approved BRAFi/MEKi combinations. Future studies are warranted to test neratinib reversal of BRAFi/MEKi resistance in patient melanomas expressing ERBB3/HER3 in combination with its dimerization partner ERBB2/HER2.

In vivo experiments showed that CD8+T cell-derived exosome miR-2682 inhibited lung cancer tumor formation, while CAF-derived exosome FOXD3-AS1 promoted lung cancer tumor formation. This study provides mechanistic insights into the role of miR-2682 and FOXD3-AS1 in lung cancer progression and provides new strategies for lung cancer treatment.

Altogether, our study suggests a possible role of lincRNA-p21 and RMST lncRNAs in the etiology of PC pathobiology, and their biomarker role may be understood in future studies.