BBOX1 (Gamma-Butyrobetaine Hydroxylase 1)

Our HRD-based prediction model offers a reliable tool for CHOL prognosis, suggesting new potential for six candidate genes as prognostic biomarkers. It highlights potential therapeutic targets and drug sensitivities, providing new insights into personalized treatment strategies for CHOL management.

Population samples and in vitro experiments further validate these findings. With high data utilization efficiency and low computational cost, MODA serves as a robust tool for uncovering novel disease mechanisms and advancing precision medicine.

Enrichment analysis of asRNAs with target mRNAs showed enrichment in biological regulation and developmental processes involved in the PI3K, p53, apoptosis, and VEGF signaling pathways. This study identified 14 asRNAs for the first time and showed that asRNAs targeting mRNAs strongly associated with tumor development in GBC through the PI3KCA and TP53 pathways.

Loss of BBOX1 in tumor cells promoted their destruction by NK cells in vitro and improved the efficacy of NK cell adoptive transfer therapy in vivo. These findings illustrate how BBOX1-positive tumor cells hijack carnitine production to evade immune surveillance during metastasis and propose BBOX1 as a potential metabolic checkpoint for anti-metastatic strategies.

TRIM31 enhances the proliferation, migration, and invasion of Eca109 cells through the ubiquitination of BBOX1. In conclusion, TRIM31 functions as an oncogene, suggesting its potential as a novel therapeutic target or prognostic biomarker for patients with esophageal cancer.

In addition, the molecular dynamics simulation, PCA/FEL, and MM/PBSA analysis conclusively evaluate the binding potential of the compounds and unequivocally stabilize specific conformations or deception of the complexes in high-energy states. Thus, the identified compounds lead to the disruption of BBOX1-IP3R3 interaction, which aids in the therapeutic option of TNBC.

Knockdown of lncRNA BBOX1-AS1 inhibits U-87 MG cell proliferation and promotes apoptosis by upregulating miR-382-5p and downregulating CBX3 expression.

This model demonstrates potential in predicting prognosis and immunotherapy response, providing insights into personalized treatment strategies for HCC. Additionally, our study suggests that BAMBI may serve as a novel biomarker and potential therapeutic target for HCC.

Mechanistically, BBOX1 disrupts TBK1 activation by preventing its interaction with the upstream activator doublecortin-like kinase 2 (DCLK2). This BBOX1-DCLK2-TBK1 axis unveils an important mechanism in ccRCC metabolic dysregulation and highlights potential therapeutic strategies.

Henceforth, the overall analysis infers that the phytocompounds CID_22217550, CID_559476, and CID_550931 shall act as potent inhibitors of BBOX1. However, their inhibitory efficacy has be to analyzed with further in vitro and in vivo analysis.

High BBOX1 expression in paracancerous tissues correlated with poor overall survival and disease-free survival in HCC patients. These findings suggest that the paracancerous BBOX1 expression might be a credible indicator for overall survival or disease-free survival in HCC patients.

Furthermore, following BBOX1 overexpression, cell proliferation and migration are decreased, the cell cycle is arrested, and ROS are attenuated. BBOX1 has suppressive effects on HepG2 cells, potentially through its ability to hinder cancer cell proliferation, arrest cell cycle progression, and decrease ROS levels, suggesting its potential as a novel prognostic biomarker and therapeutic candidate for hepatoblastoma.