TNS3 (Tensin 3)

We identified multiple AD risk-modifying genes dependent on both cellular context and APOE*4 status. These insights may inform therapeutic strategies aimed at APOE*4 and guide experimental interrogation of APOE's pathogenic mechanisms across brain cell types.

Druggability analyses nominated several potential drug targets for PCa, such as HSPB1, RRM2B, and PSCA. Our findings reveal novel risk loci and candidate protein biomarkers, providing new etiological insights and potential avenues for PCa early detection and therapy.

Clinically, tensin dysregulation correlates with metastasis and poor prognosis: TNS2 serves as a diagnostic biomarker for gastrointestinal stromal tumors, aberrant TNS1/TNS3 expression predicts metastasis risk, and TNS4 is recurrently embedded in multi-gene prognostic signatures. This review synthesizes their structural basis, regulatory mechanisms, and clinical relevance, highlighting context-dependent switches and TNS4's therapeutic potential.

The results obtained indicate the diagnostic potential of TNS3-203, but not LRRFIP1-211 transcript and its role in oral carcinogenesis.

The two-step MR study found SHBG to be a mediator between IGF-1 and PCa, and the colocalization analysis found that there was a common causal variant (nearby gene TNS3) between IGF-1 and SHBG (PPH4=93.21%), which further confirmed the mediating effect of SHBG. Strong evidence from our study suggests that IGF-1 increases the risk of PCa by decreasing SHBG levels, and in addition some BUBs were found to have a potential causal relationship with UCs.

The upregulated expression of hsa_circ_0001165 modulates the miR-381-3p/TNS3 axis and promotes aggressive phenotypes of ESCC. Hsa_circ_0001165 is regarded as a encouraging biomarker and potential therapeutic target for ESCC, presenting innovative options for both diagnostic and treatment approaches.

However, our data suggest that brain tumor lesions classifying as DNT by DNA methylation with low score represent a diverse group. Furthermore, some FCD can classify as DNT, albeit with low calibrated score and require close correlation.

Here, we will summarize what is known about the fate and functions of individual MALT1 substrates and how their cleavage contributes to the biological functions of the MALT1 protease. We will outline what is needed to better connect critical pathophysiological roles of the MALT1 protease with the cleavage of distinct substrates.

Critically, these findings have clinical relevance as TNS3 expression in EWS tumors positively correlates with that of ETS1. Implications: ETS1's transcriptional regulation of the gene encoding the focal adhesion protein TENSIN3 in Ewing sarcoma cells promotes cell movement, a critical step in the evolution of metastasis.

Moreover, silencing of Tensin-3 expression in MALT1-driven lymphoma promoted dissemination of xenografted lymphoma cells to the bone marrow and spleen. Thus, MALT1-dependent Tensin-3 cleavage reveals a unique aspect of the function of MALT1, which negatively regulates integrin-dependent B cell adhesion and facilitates metastatic spread of B cell lymphomas.

BRAF fusions have shown responses to MEK inhibitors and non-specific RAF inhibitors (eg, sorafenib) in Melanoma (NCCN)... BRAF fusions were detected in 0.2% (164/80083) of Chinese solid tumor patients. 70.1% of BRAF fusion positive cases were diagnosed with glioma and 29.9% were diagnosed with non-glioma. 14 novel BRAF fusion partners were discovered.

These results suggested that ambient PM exposure may increase the expression of miR-200 family and then promote the proliferation and migration of lung cancer cells. Our study provided novel model and insights into the molecular mechanism of ambient PM exposure-induced lung cancer.