SGK1 (Serum/Glucocorticoid Regulated Kinase 1)

Persistent high SGK1 expression, particularly discernible in individuals harboring high-risk (HR) cytogenetic profiles, was considerably associated with an elevated risk of relapse (hazard ratio for high vs. low SGK1 expression: 2.7; 95% CI: 1.4-5.3; p  < 0.01). SGK1 gene expression in PBMCs serves as a promising, minimally invasive biomarker for relapse prediction in MM individuals undergoing AHSCT.

BMBC spheroids were cultured on soft (∼0.4 kPa) or stiff (∼4.5 kPa) HA hydrogels, known to induce dormant versus proliferative states, and their response to Paclitaxel (PTX) or Lapatinib (LAP) treatment was measured. Further, SGK1 inhibition alleviated drug resistance and resulted in response to treatment. Overall, this work provides evidence for dormancy associated drug resistance through GR signaling in BMBC spheroids.

Collectively, our results highlight the protective effects of NMN against CTX-induced damage to the reproductive function, thus addressing a critical gap in fertility preservation. We present a potential non-invasive strategy that does not interfere with cancer therapy timelines.

In this review, we focus on the role of SGK1 in neurodegenerative diseases, specifically in AD. In addition, it discusses the role of SGK1 signaling pathways and the possible SGK1 as a therapeutic target in memory formation and Aβ metabolism.

The findings illustrated a transcriptional landscape of hippocampal OLs and substantiated impaired myelination in DACD. Our results provided direct evidence that inhibition of SGK1 or the promotion of myelination might be a potential therapeutic strategy for DACD.

Moreover, mechanistic studies showed that compound 12f hindered PC3 cell migration and invasion, improved the thermal stability of SGK1 protein in PC3 cells, decreased SGK1 protein levels in tumor tissues, and effectively inhibited the phosphorylation of SGK1 and its substrates in PC3 cells in a dose- and time-dependent manner. In summary, the results of this study highlight the potential of 12f as a lead compound for further optimization in the development of new therapies against PCa targeting SGK1.

Herein, we review recent literature on SGK1's primary functions within the nervous system and its impacts within different neurological disorders. We summarize significant findings, identify research gaps, and outline possible future research directions based on the current understanding of SGK1 to help further progress the understanding and treatment of neurological disorders.

It was found that cells cultured on soft HA hydrogels (∼0.4 kPa) that showed a non-proliferative (dormant) phenotype exhibited resistance to Paclitaxel or Lapatinib. Accordingly, SGK1 inhibition resulted in a dormant-to-proliferative switch and response to therapy. Overall, our study demonstrates that matrix stiffness influences dormancy-associated therapy response mediated, in part, via the p38/SGK1 axis.

SGK1 integrates a broad spectrum of effects to maintain the homeostasis of cell survival and apoptosis, conferring viability to multiple cell types as well as both simple and complex organisms, and thus ensuring appropriate prenatal development and reproductive lifespan.

Furthermore, our results clearly showed that sgk-1 was upregulated in lin-35 worms compared to N2 worms. Our results highlight the importance of definitive validation using mostly expressed reference genes.

By contrast, staining area and normalized staining were reduced for other proteins in HPV-OPSCC than control specimens. Our collective observations suggest differential cellular localization and expression of glucocorticoid-inducible proteins in HPV-OPSCC suggestive of different functional roles in pathogenesis of this condition.

The dots represent the observed logFC, the horizontal line the bootstrapped 95%Confidence Intervals; PTGDR2= prostaglandin D2 receptor 2; ns= not significant B) Differentially expressed genes in Non Responders vs Responders CD8pos naïve T cells. FDR=False Discovery Rate; CCL5= Chemokine (C-C motif) ligand 5; PRDM1= PR/SET Domain 1; SGK1= serum/glucocorticoid regulated kinase 1.