BCL2 (B-cell CLL/lymphoma 2)

Riluzole disrupts mitochondrial homeostasis by increasing Bax/Bcl-2 ratio, resulting in a drop of mitochondrial membrane potential. In conclusion, riluzole inhibits HCC growth by regulating glucose and glutamine metabolism and inducing autophagic cell death, thereby highlighting its therapeutic potential for HCC treatment.

PDHA1 status also modulates sensitivity to phenformin and the E2F1 pathway inhibitor NSC-207895. Collectively, PDHA1 orchestrates a cuproptosis-associated E2F1-PD-L1 program that promotes immune exclusion yet predicts ICB responsiveness, supporting PDHA1 as a clinically actionable biomarker and metabolic-immunologic target in sarcoma.

Genome-wide CRISPR screening identifies that loss of GPX4 and BCL2 by genetic manipulation or pharmacological treatment enhances the ability of RTTA to inhibit hepatocellular carcinogenesis. Our findings establish RTTA as a therapeutic strategy targeting tyrosine dependency and highlight combinatorial targeting of translation-metabolism crosstalk and ferroptosis pathways in liver cancer.

Additionally, the clinical use of tyrosine kinase inhibitors in some of these cases showed therapeutic efficacy. Collectively, these findings identify BCL11B-enhancer mediated deregulation of FOXF1/FENDRR as a hallmark of a subtype of high-risk lineage ambiguous leukemia that is potentially amenable to targeted therapeutic intervention.

Compound-target docking results displayed that bornyl acetate (the main components of HEO), caryophyllene oxide and terpineol had strong binding interactions with the active sites of PI3K and Akt, indicating they contribute to the therapeutic effect. These results demonstrated that HEO exerts anti-tumor effects in DLBCL via suppressing PI3K/Akt signaling pathway, indicating HEO may be a potential inhibitor of PI3K/Akt signaling pathway for the treatment of DLBCL.

Moreover, in in vivo assays, USP4 independently promoted cell proliferation, sustained stemness and enhanced mitochondrial function, thereby increasing tumor growth. Collectively, the findings of the present study revealed that AL445238.2, through its interaction with USP4, orchestrated the regulation of cell proliferation, apoptosis, stemness maintenance and migration in CRC cells, offering novel insights into the role of lncRNAs in cancer progression and highlighting potential therapeutic targets.

The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 41: 3069‑3079, 2019; DOI: 10.3892/or.2019.7070].

The research findings validate ETP-DNP as a promising nanocarrier system for ‎breast cancer. ‎.

Its overexpression correlates with poor prognosis and represents a potential diagnostic and therapeutic target. Furthermore, targeting TNFRSF10B may restore apoptosis, thus making precision therapy achievable.

C. spinosa extract induces mitochondrial apoptosis and inhibits PC3 proliferation, supporting its potential as a phytotherapeutic candidate.

Integrated mechanistic studies, including network pharmacology, transcriptomics, and Western blot analysis, indicated that the anti-leukemic effects of oleandrin are associated with suppression of the PI3K/AKT signaling pathway, as evidenced by reduced levels of key proteins such as PIK3CA, phosphorylated AKT (p-AKT), phosphorylated GSK3β (p-GSK3β), c-Myc, Bcl-2, and Bcl-xL. These findings suggest oleandrin is a promising therapeutic candidate for T-ALL, likely through suppression of the PI3K/AKT pathway.

Key targets like B-cell lymphoma 2 (BCL2) and caspase-3 (CASP3) were identified, with enrichment analyses highlighting xenobiotic response, protein phosphorylation, advanced glycation end product-receptor for advanced glycation end product (AGE-RAGE) signaling, insulin resistance, and apoptosis pathways. The findings suggest PAEs disrupt metabolism via apoptosis, inflammation, protein kinase alterations, and neuroendocrine interference, underscoring the global health risks posed by endocrine disruptors from food packaging.