BNIP3L (BCL2 Interacting Protein 3 Like)

Specifically, we explore the metabolic bridges linking HIF and autophagy, including glycolysis and reactive oxygen species (ROS). Furthermore, by refining the content of dual-target molecules, we propose strategies for co-targeting HIF and autophagy, aiming to catalyze the development of novel therapeutic interventions.

Elevated BNIP3L levels were significantly associated with adverse clinical characteristics, suboptimal treatment response, and a trend toward inferior survival. Consequently, measuring serum BNIP3L could be valuable for monitoring disease progression and prognostic evaluation in MM patients.

These findings indicate heightened inflammation and upregulation of mitophagy pathways in the adipose tissue of individuals with obesity. The upregulation of mitophagy-related genes seems to indicate a possible activation of mitophagy-associated pathways in the altered metabolic and inflammatory environment of obesity.

According to our data, mitophagy is responsible to IR but plays a very limited role in the radiosensitivity of adenocarcinoma cells. Further in vivo studies are warranted to elucidate the radiosensitizing effect of targeting mitophagy on malignant tumors.

In summary, our findings establish that BNIP3/BNIP3L-mediated mitophagy, driven by DNA-PK-dependent NF-κB hyperactivation, is essential for CSC maintenance. Targeting the DNA-PK/NF-κB/BNIP3L-BNIP3 axis to disrupt mitochondrial quality control in CSCs represents a promising therapeutic strategy to prevent ovarian cancer recurrence and metastasis.

The review also explicates the significance of healthy mitochondria and normally functioning mitophagy in Alzheimer's. Finally, the review states the implications of BNIP3L in other diseases, like cardiovascular conditions and cancer, underscoring the immense potential of this wonder protein.

Taken together, our findings may contribute to the treatment and prognosis prediction of MM patients.

This process facilitates the expression of U-rich genes, such as mitophagy-related genes FUNDC1, BNIP3L, thereby maintaining cellular homeostasis and promoting cell survival under adverse conditions. Our findings reveal that PABPC1 SUMOylation connects stress granule assembly with selective U-rich mRNA stabilization and mitophagy, promoting cancer cell stress adaptation.

We confirm that miR-92a-1-5p regulates proliferation and cell cycle by targeting TP53INP1 and decreases autophagy by targeting BNIP3L. Our data suggest that miR-92a-1-5p plays a role in CML progression, and its inhibition enhances imatinib anti-leukemic efficacy, making it a potential therapeutic target.

Notably, GBE1 emerged as a significant gene, impacting both patient survival and the most immune cell infiltration. Hence, further studies are warranted to elucidate its precise mechanisms and explore its potential as a therapeutic target in cancer immunotherapy.

We used a powerful machine learning framework to highlight the great potential of MacPCD in providing personalised risk assessment and immunotherapy intervention recommendations for KIRC patients.