BNIP3 (BCL2 Interacting Protein 3)

In vitro experiments using the HK-2 cell line provided further evidence supporting the in vivo findings. The pathogenesis of clinical-dose ATO-induced AKI involves OPA1- and Drp1-mediated mitochondrial dynamics imbalance and PINK1/Parkin-dependent mitophagy in renal tubular epithelial cells, CHF ameliorated this injury by restoring mitochondrial quality control, highlighting its therapeutic potential against AI-AKI.

According to the study findings, BNIP3 expression is lower in breast cancer and may influence the prognosis and play a role in immune modulation. Our findings suggest that hypoxia and immune response regulate the expression of BNIP3 in breast cancer. Hence the results signify the importance of BNIP3 as a prognostic marker in breast tumor progression.

LCFE exerts an anti-tumor effect by activating apoptosis and autophagy processes in breast cancer cells, while having low cytotoxicity for normal breast cells, highlighting the potential of LCFE as a natural agent for cancer treatment.

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.

Drug sensitivity analysis suggests that tumors with high BNIP3 expression are sensitive to IGF-1R/p53 inhibitors, while those with low expression respond to mTOR inhibitors. In summary, BNIP3 promotes BC progression by driving glycolysis and an immunosuppressive microenvironment, and can serve as an independent prognostic biomarker and a potential therapeutic target.

In addition, autophagy-related biomarkers (sequestosome 1, LC-3B and beclin-1) are associated with clinical outcomes and may guide patient stratification. Given the bidirectional nature of selective autophagy in HCC, personalized approaches based on tumor context, specific pathway dependencies and disease stage are essential for effective therapeutic intervention.

Moreover, pharmacological inhibition of HDAC with Trichostatin A (TSA) suppressed both HDAC6 and BNIP3 expression, decreased autophagic activity, and reduced lung tumor formation in a KRASG12D+/P53loxP/loxP transgenic mouse model. Collectively, these results reveal a novel HDAC6-HIF-1α-BNIP3 axis that governs autophagy in lung cancer and underscore the potential of HDAC6 as a therapeutic target for modulating autophagy and inhibiting lung tumor progression.

Cisplatin-resistant NSCLC cells with different treatments were ectopically grown with rapamycin (RAPA) interventions, and the tumor growth rate was examined in vivo. Finally, we confirmed that TFAP2A silencing can inhibit tumor growth in vivo through experiments on xenograft tumor model of nude mice. TFAP2A overexpresses significantly in NSCLC, and promotes cisplatin resistance through BNIP3-mediated mitophagy.

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.

Finally, assessment of bone marrow CD8+ T cells from multiple myeloma patients identified decreased proliferation, c-Myc and Rheb expression compared to peripheral blood cells, alongside elevated BNIP3, confirming mechanistic features of hypoxic exposure in this environment. Taken together, the findings indicate potential for bone marrow hypoxia to influence efficacy of T cell-directed therapies for multiple myeloma.

Furthermore, JA enhanced cytotoxicity of T24 cells to anti-cancer drugs cisplatin combined with gemcitabine. Analyses of patients' data further showed that, in contrast to other major cancer types, lowered mitophagy in bladder urothelial carcinoma compared with normal tissues and reduced expression of mitochondrial genes in cisplatin-responsive bladder cancer cells compared with non-responsive cells suggest mitophagy acts as a tumor suppressor to avoid cisplatin resistance in bladder cancer. Overall, our data suggest the role of BNIP3 and mitophagy in anti-cancer mechanism of human bladder cancer with HRAS mutation in response to JA.

BNIP3 overexpression inhibits RCC progression by promoting HIF-1α-mediated autophagy and subsequent apoptosis under hypoxic conditions, primarily through disrupting the Bcl-2/Beclin1 complex. These findings establish BNIP3 as a potential therapeutic target for RCC, warranting further investigation into autophagy-based interventions.