TCF7L2 (Transcription Factor 7 Like 2)

Taken together, our findings identify MASLD as a modifiable risk factor for neurodegeneration, with systemic inflammation playing a pivotal role in the liver-brain axis. This study highlights key genes and pathways underlying MASLD-induced cognitive impairment, advances understanding of metabolic-neural cross talk, and offers potential therapeutic targets for mitigating cognitive decline through intervention in the liver-brain axis, developing intervention strategies and highlight the therapeutic promise of targeting the liver-brain axis.

Functionally, TCF7L2 maintained proliferation via the MAPK signaling axis in this subtype of CRPC. Together, these data provide a mechanistic rationale for interventions that perturb DNA binding of the pro-proliferative transcription factor TCF7L2 and/or direct MAPK signaling inhibition in the CRPC-WNT subclass of advanced prostate cancer.

Overall, our results provide genetically-underpinned molecular mechanism through which promising treatments for PD may work.

Additionally, Western blot and experiments employing the PI3K inhibitor LY294002 have demonstrated that TCF7L2 activates the PI3K/AKT signaling pathway, thereby facilitating the proliferation of CRC cells...Spearman correlation analysis confirmed a positive relationship between the expressions of TCF7L2 and HIF-1α, while Kaplan-Meier survival analysis demonstrated that their co-expression was predictive of reduced overall survival. Collectively,these findings position TCF7L2 as a critical downstream effector of HIF-1α in hypoxic CRC, and its mechanistic role in promoting malignancy and correlation with poor prognosis provide a theoretical basis for exploring TCF7L2 as a potential therapeutic target in future studies..

Mutational signatures implicate ROS (SBS18), HR deficiency (SBS3), and SBS8 across ≥9 cancer types. These results establish foundational insights into PM biology, though future PM tissue profiling is warranted to overcome primary tumor bias in genomic data.

The levels of inflammatory factors IL-6, TNF-α, and TGF-β(1) and the expression level of protein iNOS were significantly decreased (P<0.05) . miR-204-5P alleviates SiO(2)(-) induced macrophage inflammation by regulating the wnt/β-catenin pathway and JAK2/STAT3 pathway.

Nonetheless, GLN therapy significantly alleviated testicular impairments via regulating aforementioned biochemical and histological abnormalities. These findings suggest he palliative efficacy of GLN against DPN induced testicular damages thereby recommending the use of GLN to promote reproductive health in male.

This study identified CRC-linked genes through GWASs and transcriptomics, highlighting their prognostic and druggable relevance. Computational drug repurposing pinpoints PYGL inhibitors as promising candidates, offering a translational framework for CRC therapy development.

Our results reveal a distinct mutational profile in Saudi CRC patients, characterized by novel and enriched somatic variants affecting key oncogenic pathways. These findings underscore the necessity of including underrepresented populations in cancer genomics to support globally equitable precision oncology.

β-Catenin, crucial in gene regulation for cell proliferation and differentiation, is a key target in cancer therapeutics. Confirming focal molography's ability to accurately measure binding affinities creates a reliable methodology that fills gaps in current drug discovery techniques.

Peptostreptococcus stomatis activates integrin α6/β4→ERBB2-MAPK and can bypass targeted inhibitors, while Parvimonas micra enhances WNT/β-catenin programs and Th17-skewed immunity. Together, these data support a systems view in which microbial cues and host epigenetic control jointly drive CRC initiation, progression, metastasis, and treatment response.

Indeed, we found that miR-29b1~a expression is inversely correlated with SPARC levels, and it is significantly reduced in samples with a mesenchymal-like phenotype. Taken together, SPARC expression in melanoma cells relies on transcriptional activation by PRRX1/TCF7L2-Sp1 and is modulated through miR-29b1~a, which provides fine-tuning regulation over the switch between phenotypic states.