GNG4 (G Protein Subunit Gamma 4)

This process promotes prostate cancer progression and resistance to androgen receptor signaling inhibitors (ARSis). In contrast, GNG4 knockdown or pharmacological inhibition of autophagy restores ARSI sensitivity and suppresses tumor growth.

The three-gene MDG-based prognostic model effectively predicts survival outcomes in LIHC patients. Moreover, the methylation status of GLS serves as a biomarker for assessing immune microenvironment characteristics, responsiveness to immunotherapy, and chemotherapy sensitivity, highlighting its potential as a therapeutic target in liver cancer.

The prognostic value of GNG4 was further validated in AML patient samples through qRT-PCR.ConclusionClinical validation indicated a substantial downregulation of GNG4 in AMLNPM1mutFLT3-ITDmutDNMT3Amut compared to AMLNPM1mutFLT3-ITDmutDNMT3Awt patients. Thus, GNG4 may play a role in the low survival rate of AMLNPM1mutFLT3-ITDmutDNMT3Amut patients, offering novel insights into the prognosis, therapeutic targets, and prognostic evaluation of AML.

We next performed functional enrichment analysis which revealed that immune response and metabolic processes play a pivotal role in cervical cancer. Our large scale scRNA-seq of cervical cancer provide insights into cellular heterogeneity and gene expression dynamics within the tumor microenvironment.

These findings indicate that both glucose and insulin can elicit inflammatory responses in BV2 cells through the modulation of mmu_circ_0010164 levels. The underlying mechanism may involve potential downstream targets of mmu_circ_0010164, specifically mmu-miR-7043-3p/Gng4 and mmu-miR-6918-3p/Mterf1b. This provides novel insights into the treatment of glucose-induced neuroinflammation.

This analysis study identified the hub genes and associated pathways involved in the pathogenesis of UCEC. The identified hub genes exhibit remarkable potential as diagnostic biomarkers, providing a significant opportunity for early diagnosis and more effective therapeutic approaches for UCEC.

Treatment with a cGAS-STING pathway inhibitor reversed the inhibition of proliferation, migration, and invasion while downregulating the expression of pyroptosis-related proteins. Silencing GNB4 promotes pyroptosis and thus inhibits the proliferation, migration, and invasion of glioma cells by activating the cGAS-STING pathway, which is a promising biomarker and therapeutic target for glioma.

GNG4 expression predicted the immunotherapy response in the IMvigor210 cohort, suggesting that GNG4 could be used as a potential biomarker in CC for prognostication and immunology. Moreover, the expression of GNG4 predicted the immunotherapy response of ICB in CC.

In addition, CRISPR screening to identify molecules associated with elevated MHC-I expression independent of IFNγ signaling pathways demonstrated that guanine nucleotide-binding protein subunit gamma 4 (GNG4) maintained MHC-I expression via the NF-κB signaling pathway. Our results indicate that patients with IFNγ signaling pathway defects are not always resistant to immune checkpoint inhibitors and highlight the importance of MHC-I expression among the pathways and the possibility of NF-κB-targeted therapies to overcome such resistance.

In addition, clustered regularly interspaced short palindromic repeats (CRISPR) screening to identify molecules with elevated MHC-I expression independent of IFN-γ signaling pathways demonstrated that guanine nucleotide-binding protein subunit gamma 4 (GNG4) maintained MHC-I expression via the NF-κB signaling pathway. Our results indicate that patients with IFN-ɤ signaling pathway defects are not always resistant to ICIs, and highlight the importance of MHC-I expression among the pathways, including inhibitory effects on cellular proliferation or chemokine production, and the possibility of NF-κB-targeted therapies to overcome such resistance.

Through bioinformatics analysis and experimental verification, high expression of GNG4 in osteosarcoma was identified as an oncogene and reliable biomarker for poor prognosis. This study helps to elucidate the significant potential of GNG4 in carcinogenesis and molecular targeted therapy for osteosarcoma.

High levels of NMU, PPBP, and GNG4 were associated with poor prognosis in CC. The combination prognostic model of these three genes could be a new option.