BMI1 (BMI1 proto-oncogene, polycomb ring finger)

These findings provide mechanistic insight into how aberrant DNA methylation drives HSC dysfunction in MDS and offer an epigenomic resource for discovering regulators and therapeutic targets at the stem cell level. The online version contains supplementary material available at 10.1007/s44466-026-00034-4.

Blue light irradiation reduced viability and migration in both OSCC cell lines and induced apoptosis only in non-metastatic SCC9 cells. Blue light exerted anti-tumor effects without promoting cancer stem cells properties, while decreasing their ability to self-renew.

Cadmium exposure may initiate and promote brain tumour development by regulating SHH, GLI1, BMI1 and TP53. This may disrupt the normal regulatory mechanisms of the SHH-GLI1 pathway.

Together, these findings demonstrated that the PAK5-HMGCS2 pathway drives breast cancer metastasis and can be circumvented using a KD. PAK5-mediated phosphorylation of HMGCS2 promotes breast cancer growth and metastasis by inhibiting β-hydroxybutyrate production, revealing the role of PAK5 in ketone metabolism and highlighting a potential therapeutic target for breast cancer metastasis.

Notably, a clinical trial incorporated stem cell markers as surrogate end points for evaluating treatment options. While findings underscore the prognostic and therapeutic relevance of stem cells in OPMD, lack of prospective designs in biomarker validation and absence of clinical trial evidence on stem cell therapies limit clinical applicability.

iPSC-MSC-Exos ameliorated colitis and promoted mucosal healing in a TNBS-induced CD-like model by activating Wnt/β-catenin signaling via miR-34a-5p, which targets PPP2R3A.

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.