PCK1 (Phosphoenolpyruvate Carboxykinase 1)

TAZ modulates gluconeogenesis and accelerates tumor growth, whereas its knockdown attenuates tumor progression. TAZ interacts with GR, suppressing its transcriptional activity on gluconeogenic gene promoters.

Estradiol administration in androgen‑deprived male mice produces a constellation of metabolic derangements-including enhanced hepatic gluconeogenesis, impaired TG clearance, and inflammatory adipocyte hypertrophy-that likely underlie the increased CVD risk observed clinically. The identified molecular nodes (PEPCK, hepatic lipase, LRP1, LDLR, MTP, and adipose‑macrophage TNFα) provide potential targets for mitigating estrogen‑induced CVD risk while preserving its therapeutic benefit for PrCa.

These results indicate PCK1 is a key lactate metabolism-related tumor suppressor in iCCA. PCK1 exerts its anti-tumor effects by coordinately suppressing lactate accumulation and inhibiting the PI3K-AKT signaling pathway, positioning it as a promising diagnostic biomarker and therapeutic target for iCCA.

Overall, PN modulates macrophage-fibroblast interactions via the CREB/PCK1 axis, enhancing collagen synthesis and counteracting age-related skin changes. PN has emerged as a promising therapeutic agent for skin rejuvenation by targeting cellular senescence and promoting extracellular matrix restoration.

KLX also improved glutathione metabolism by modulating the expression of PCK1, xCT, and glutathione peroxidase 4 (GPX4)-related proteins. These findings demonstrate that KLX exerts potent antifibrotic effects by regulating glutathione metabolism and promoting ECM degradation, suggesting its potential as a therapeutic candidate for liver fibrosis.

Overexpression of PCK1 inhibited cellular inflammation and fibrotic changes induced by pIgA1, demonstrating protective effects against cellular fibrosis similar to rosiglitazone. PCK1 exerted a pronounced inhibitory effect on mesangial cell inflammatory markers and fibrosis indicators in IgAN, potentially offering a novel therapeutic target for its treatment.

Increased expression of these genes in fly, mouse, and human correlates with poor prognosis, and hepatic expression of Pdk3 emerges as a previously unknown mechanism contributing to metabolic dysfunction in cancer cachexia. This study highlights the conserved nature of tumour-induced metabolic disruptions and identifies potential therapeutic targets to mitigate cachexia in people with cancer.

However, PS-NH2 strongly competes with hydrogen bonds of the first rate-limiting enzyme PCK1 in gluconeogenesis, thus downregulating the expression of PCK1 and promoting the aerobic glycolysis pathway, which most tumor cells prefer. This study indicates that positive-charge modified NPs in the environment may bring additional carcinogenic risks.

SIRT2 inhibits articular chondrocyte extracellular matrix (ECM) degradation, inflammatory factor expression, and apoptosis via PCK1.

Downregulation of TBL1X in HepG2 cells and the TBL1X N365Y variant in iHeps have differential effects on T3 regulated gene expression. This suggests that TBL1X may play a gene context role in thyroid hormone TH action.

This research investigated breast cancer liver metastasis relapse by employing a comprehensive approach that integrated data filtering, gene ontology and KEGG pathway analysis, overall survival analysis, identification of the alteration in the DEGs, visualization of the protein-protein interaction network, Signor 2.0, identification of positively correlated genes, immune cell infiltration analysis, genetic alternation analysis, copy number variant analysis, gene-to-mRNA interaction, transcription factor analysis, molecular docking, and identification of potential treatment targets. This study's integrative approach unveiled metabolic reprogramming, suggesting altered PCK1 and LPL expression as key in breast cancer metastasis recurrence.

Moreover, overexpression of Pck1 alone or together with Ppara in vivo lowered hepatic triglycerides and steatosis. Our data support the notion that the IF 5:2 regimen is a promising intervention against NASH and subsequent liver cancer.