G0S2 (G0/G1 Switch 2)

A VM-related model was constructed to assess the prognosis and therapeutic efficacy in patients with GBM, contributing to the management of GBM in clinical practice.

P1, N=64, Recruiting, Mayo Clinic | Trial completion date: Dec 2025 --> Dec 2026 | Trial primary completion date: Dec 2025 --> Dec 2026

This was also sufficient to delipidate classical adipose depots and was recapitulated in tumour-associated cachexic mice. Overall, this defines unique adaptations of stable adipocytes to resist lipolysis in healthy states while isolating a potent catecholamine-independent neurosystemic pathway by which the body can rapidly catabolize all adipose tissues.

Mechanistically, FFAs were found to trigger Akt activation, and pharmacological inhibition of this protein by BEZ235 could successfully counteract their cancer-promoting effects. Collectively, these results support the presence of an EV-driven bidirectional interplay between PCa cells and adipocytes, which reprograms the latter toward a lipolytic, tumor-promoting phenotype.

Palmitate treatment resulted in significant sensitization to radiation treatment and enhanced the efficacy of poly (ADP-ribose) polymerase (PARP) inhibitors. In summary, we demonstrate that G0S2-dependent lipid metabolism regulates cell cycle phase-specific radiation sensitivity of HNSCC cells and identify G0S2 and free fatty acids as novel targets for radiation therapy.

SRC inhibition or G0S2 silencing completely abolished TNBC cell chemoresistance driven by ECM-myCAFs. Altogether, this work reveals the unique role of the specific ECM-myCAF population and identifies G0S2 as a key player in chemoresistance in TNBC.

This study reveals the molecular characteristics of key prognostic factors in GBM, highlighting the importance of immune cell abundance and drug sensitivity in glioma treatment, and provides potential biomarkers and therapeutic targets for future clinical research and treatment strategies.

This study highlights the role of FAM in IS, identifies VIM, G0S2, and GPR84 as novel diagnostic biomarkers, and positions GPR84 as a therapeutic target, thereby advancing precision diagnosis and treatment.

Tumor microenvironment profiling has revealed that the high-risk patients display elevated stromal and immune scores, alongside reduced tumor purity, indicative of a densely infiltrated, macrophage-rich microenvironment. By elucidating the interaction between ICD and macrophage biology, this study establishes a robust prognostic model that surpasses traditional clinical parameters, offering insights into tumor microenvironment immunity and therapeutic vulnerabilities in GBM.

In this review, we provide an overview of the current knowledge on G0S2, highlighting its regulation at different levels and unveiling its potential as a diagnostic and prognostic marker in immune-related diseases and cancer. The discussion covers the roles of G0S2 in lipolysis, lipid synthesis, inflammation, and various cancers.

Clinical validation confirmed that elevated BIRC3 and G0S2 expression correlated with poorer prognosis, while functional assays demonstrated that G0S2 inhibition suppressed tumour progression and reduced Treg infiltration in vivo. These findings position G0S2 as a promising biomarker for immunotherapy response and a potential therapeutic target, providing insights into Treg-mediated immune regulation and advancing personalized NSCLC treatment strategies.

G0S2 knockout activated the type I interferon signaling pathway, enhanced CD8+ T cell functionality, and synergized with anti-PD-1 therapy, resulting in suppressed tumor growth and prolonged survival in vivo. These findings provide a comprehensive analysis of glioma metabolic patterns and identify G0S2 as a promising therapeutic target.