THAP1 (THAP Domain Containing 1)

Based on these interactions, we hypothesise that these lncRNAs may contribute to the modulation of the GABAergic pathway, which plays a crucial role in fulfilling the high energy demands of cholangiocarcinoma cells. Further experimental validation and investigation into the regulation of SLC6A12 and GAD1 are required to gain deeper insights into CCA pathogenesis and to identify potential therapeutic targets.

Allelic combination CAG (rs4833095/ rs4986790/ rs187084) increased the risk of cervical cancer. In conclusion, the present study identified that polymorphisms in TLRs genes can affect the phenotype of their respective genes and contribute to the development of HSIL or cervical cancer.

Overexpressed MS4A3 enhances the chemosensitivity of NSCLC cells to osimertinib, whereas MS4A3 knockdown exerts the opposite effects...In conclusion, MS4A3 functions as an anti-tumor gene in NSCLC. MS4A3/THAP1/EGFR signaling enhances the chemosensitivity of lung cancer to EGFR tyrosine kinase inhibitor (TKI).

CircNRD1 overexpression significantly blocked tumor growth in vivo. CircNRD1 suppressed the proliferation and metastasis of GC cells in vitro and blocked tumor growth in vivo via modulating miR-421/THAP11 axis.

Validating the therapeutic relevance of dependencies, small-molecule inhibitors of SHP2, encoded by PTPN11, have potent preclinical efficacy against chordoma. Our results generate an emerging map of chordoma dependencies to enable biological and therapeutic hypotheses.

Additionally, using GEPIA, was observed a significantly high of IL-1β, IL-18 and TNF-α expression in cervical cancer tissues compared to normal tissues. These finds indicate that polymorphisms in the TLR4 and TLR9 genes can affect intracellular signaling and, consequently, change the patterns of the immune response, leading to an increased risk for cervical cancer.

Strikingly, THAP1F81L exhibits normal DNA binding but causes a significantly reduced DNA binding of YY1, its transcriptional partner that also has an established role in oligodendrocyte lineage progression. Our results suggest a model of molecular pathogenesis whereby THAP1F81L normally binds DNA but is unable to efficiently organize an active transcription complex.

Applying GAG-degrading enzymes or overexpressing β-glucuronidase rescues Thap1 OL maturation deficits in vitro and in vivo. Our studies establish lysosomal GAG catabolism within OPCs as a critical mechanism regulating oligodendrocyte development.