BMI1 (BMI1 proto-oncogene, polycomb ring finger)

This study confirms that short-term BMI trajectories before and after diagnosis, as well as early during treatment, are independent prognostic factors for both overall survival and progression-free survival in pancreatic cancer patients. Particular attention should be paid to patients who are normal-weight at diagnosis but transition to a low-BMI category shortly after treatment, as they face the highest mortality risk.

Collectively, our findings establish ZNF711 as a critical regulator of ENZR that promotes resistance by dually modulating the AR signaling pathway via transcriptional activation and epigenetic demethylation. Targeting the ZNF711-AR axis represents a novel therapeutic strategy to overcome ENZR in prostate cancer.

Our data demonstrated that CD80 modulated tumor-cell stemness and malignant phenotype while restraining antitumor T cell immunity. Targeting CD80 augments antitumor immunity and provides a compelling strategy to enhance treatment responses to neoadjuvant chemoimmunotherapy in HNSCC.

Recent studies indicate that multiple Ubiquitin-Specific Proteases (USP) family members play pivotal roles in lung cancer: Ubiquitin-Specific Peptidase 7 (USP7) promotes proliferation and osimertinib resistance in non-small cell lung cancer by stabilising proteins such as ERβ, c-Abl, and KRAS; Ubiquitin-Specific Peptidase 9, X-linked (USP9X) mediates radiotherapy resistance by regulating KDM4C and REV1; USP10 influences cellular metabolism and chemotherapy sensitivity via PTEN/AKT/mTOR and HDAC6 pathways; Ubiquitin-Specific Peptidase 14 (USP14) enhances tumour migration by regulating β-catenin and Acf7 stability; Ubiquitin-Specific Peptidase 22 (USP22) amplifies tumour stem cell properties and suppresses ferroptosis via EGFR and BMI1 signalling; Ubiquitin-Specific Peptidase 35 (USP35) and Ubiquitin-Specific Peptidase 38 (USP38) respectively modulate apoptosis resistance and proliferation through BIRC3 and KLF5; while Ubiquitin-Specific Peptidase 39 (USP39) influences mitochondrial metabolism via PDHA, thereby promoting tumour growth...It further explores the potential value of small-molecule inhibitors targeting USPs (such as P5091, IU1, and gentiopicroside) in reversing drug resistance, inducing apoptosis, and enhancing immunotherapy...This paper reviews the molecular mechanisms and targeting strategies of USPs in lung cancer based on a systematic literature search of PubMed and Web of Science databases. It further explores their potential applications in precision lung cancer therapy, providing theoretical foundations and directional guidance for future research.

Importantly, the dual-targeting design produced a synergistic therapeutic effect superior to free cisplatin or single-component formulations. This hybrid drug delivery system, combining calcium carbonate and cisplatin with Bmi1 siRNA, presents a promising approach for overcoming chemotherapy resistance in HCC.

Furthermore, we demonstrated that PP7080 may enhance cancer stemness features by counteracting the tumor-suppressive effect of miR-601. Targeting PP7080 may offer a promising therapeutic strategy for oral cancer by reducing cancer stemness.

Furthermore, CKMT1B overexpression facilitated lipid accumulation and stemness, effects that were reversible by the lipase inhibitor Orlistat...In functional rescue experiments, PITX2 knockdown significantly reduced lipid accumulation and stemness, while these effects were partially restored by CKMT1B overexpression. PITX2 promotes lipid accumulation and enhances stemness in LUAD cells by transcriptionally activating CKMT1B, suggesting the PITX2/CKMT1B axis as a potential therapeutic target for LUAD treatment.

The first-time exploration of molecular mechanism has revealed Bmi1 mediated Sox2/Slug/Vimentin signaling in NB progression that is inhibited by our nanohybrids. Thus, the present study divulges the immense potential of HSA-Chitosan nanohybrids as the new delivery system for nucleic acid having the promising caliber to be anti-GD2 decorated targeted epigenetic therapeutics in the treatment of NB.

Moreover, thiostrepton treatment sensitized the CTCL cells to proteasome inhibitor bortezomib, promoting apoptosis and autophagy. Collectively, these findings demonstrate that FOXM1 targeting disrupts the metabolic status and stemness features of CTCL cells via JNK activation, thereby offering novel insights into potential therapeutic strategies for overcoming therapeutic challenges in CTCL.

Flow cytometry was used to assess apoptosis, DNA damage and cell proliferation following treatment with either 15 µM ivacaftor or 30 µM carboplatin at 24, 48 and 72 h. ROR1 signalling associated oncogenic pathways including the BMI-1 and the PI3K/AKT pathways were modulated following ivacaftor treatment. In summary, ivacaftor demonstrated significant anti-tumour potential in preclinical HGSOC models, supporting its further investigation as a repurposed therapy for ovarian cancer.

We found that BMI1 affects the H2Aub on both H2Aub/H3K27me3 and only-H2Aub marked genes, whereas genes marked only by H2Aub largely depend on RING1A/B. Our data also show specific subsets of genes in which H3K27me3 levels are partially maintained by the RING-domain proteins independently of their catalytic activities, and other subsets of genes where BMI1s assist RING1s' activities for H2Aub marking, highlighting their unique and common functions.