PRKAB1 (Protein Kinase AMP-Activated Non-Catalytic Subunit Beta 1)

A 50-gene response signature, derived from integrated modeling across all platforms, predicts ∼50% reduction in recurrence and mortality risk. Like immunotherapy, CANDiT resurrects a physiologic program-differentiation-to selectively eliminate CSCs, offering a scalable, precision framework for lineage restoration in solid tumors.

Our findings reveal numerous plasma proteins linked to metabolic-related diseases. These findings offer fresh insights into the etiology, diagnostics, and treatment of these conditions.

This underscores the importance of circadian clock genes in astrocytic tumor progression and highlights their potential as biomarkers and therapeutic targets. Further research is needed to validate these results and explore their clinical implications.

Our analyses suggest an association of genetically determined abnormal glycemic traits with squamous cell lung cancer. The potential association between PRKAB1 activation and a reduced risk of developing lung adenocarcinoma appears to be independent of the anti-obesity effects of metformin, suggesting that PRKAB1 activation may have a direct protective effect on lung adenocarcinoma development.

The star target of metformin, PRKAB1, does not exhibit a substantial causal association with the risk of BC. Conversely, metformin, acting as an inhibitor of ETFDH and GPD1L, may potentially elevate the likelihood of developing ER-positive BC and HER2-negative BC. Consequently, it is not advisable to employ metformin as a standard supplementary therapy for BC patients without T2D.

Some glucose-lowering drugs were associated with gastrointestinal cancer risk, which might provide new ideas for gastrointestinal cancer treatment.

Our study highlights the necessity of performing individual validation of candidate hits from genome-wide CRISPR screens. Further studies are needed to assess the generalizability and translational potential of these findings.

This study highlights the use of daucosterol as a promising therapeutic drug for MM treatment. These data provide new insights into the potential mechanism of daucosterol in the treatment of MM, which may provide references for subsequent research and even the clinical treatment.

The results showed that inhibition of USP7 increases expression of the AMPK beta (PRKAB1), caspase 7(CASP7), and protein phosphatase 2 subunit B R3 isoform (PPP2R3A), while attenuating expression of C subunit of vacuolar ATPase (ATP6V0C), and peroxisomal biogenesis factor 11 beta (PEX11B). In summary, these findings reveal an important role of USP7 in regulating melanoma progression via PI3K/Akt/FOXO and AMPK signaling pathways and implicate USP7 as an attractive anticancer target for melanoma.