UQCRB (Ubiquinol-Cytochrome C Reductase Binding Protein)

This study provides a comprehensive analysis of METCGs in LGG and develops a robust prognostic model for patient stratification. SDHB, a key subunit of Complex II, plays a crucial role in mitochondrial function and tumor progression. Our findings suggest that he high expression of SDHB in LGG contributes to maintaining elevated SDH and Complex II activity, ensuring the structural and functional integrity of mitochondrial ETC complexes. This supports the high ROS production and MMP required for the rapid growth of LGG, thereby promoting its proliferation and invasion. Thus, targeting SDHB and its associated pathways could offer new therapeutic avenues for LGG treatment.

Notably, SFXN4 was found to be highly expressed in osteosarcoma tissues and cells; it promoted the growth, migration, and invasion of osteosarcoma cells, while SQOR had the opposite effect. Our research has developed a robust hypoxia- and lactate metabolism-related gene signature, providing a solid theoretical foundation for prognosis prediction, classification of "cold" and "hot" tumors, accessing immunotherapy response, and directing personalized treatment for osteosarcoma.

Our study confirms a 5-gene signature as a key biomarker for ICI response in NSCLC, enhancing treatment precision.

These findings were validated using The Cancer Genome Atlas Prostate Adenocarcinoma (TCGA-PRAD) dataset, as well as through histological and cytological experiments. The results presented here establish a foundation for ST-based evaluation of GS progression and provide valuable insights into the GS progression-related genes UQCRB and LBH.

Patients in low ASR group responded more actively to traditional chemotherapy drugs (Erlotinib and Roscovitine). CellChat analysis revealed that high ARS cell groups communicated with immune cells via SPP1 (ITGA4-ITGB1) and MK (MDK-NCl) signaling pathways. In this research, integrative analysis based on the ARS model provided a potential direction for improving the diagnosis and treatment of LUAD.

The detailed regulatory mechanism that links HOXD10 and the oxidative phosphorylation genes is not yet fully understood, our findings provide novel insight into HOXD10-mediated pathways and their effects on cancer metabolism, carcinogenesis, and the progression of EOC. Thus, the data suggest that strategies to interfere with metabolism-related pathways associated with cancer drug resistance could be considered for the treatment of ovarian tumors.

Finally, using cellMiner database and molecular docking, it was confirmed that UQCRB binds covalently to Amonafide via lysine at position 78 and threonine at position 82, while cellular assays showed that Amonafide inhibits glioma migration and invasion. Our three mitochondrial genomic composition-related features accurately predict Survival in glioma patients, and we also provide glioma chemotherapeutic agents that may be mitochondria-related targets.

Our results confirm the pivotal role of UQCRB in hypoxic signaling inducing EMT. Thus, UQCRB might be a new therapeutic target for the development of drugs able to reverse EMT by blocking mitochondrial ROS production.

Aspirin, metformin, atrovastatin, thrombin, androgen and antiandrogen drugs, progesterone, Vitamin D, and Ginsengoside 20(S)-Protopanaxadiol were also documented. A bioinformatic data mining strategy identified several anticancer, immunomodulator, and other candidate drugs that may affect the risk of BRONJ in cancer patients.