POU5F1 expression

Multi-omics and tissue analyses identified VHL as the most consistent risk gene, supported by colocalization, TCGA HNSC transcriptomic validation (P < 0.01), and DepMap functional data. GEN1 and POU5F1 expression in salivary gland tissue also associated with OCC risk.ConclusionThis multilayer SMR study reveals causal links between DNA repair-related genes and OCC, highlighting VHL as a key driver and suggesting targets for early detection and precision therapy.

Importantly, we demonstrate that RX-5902, a Wnt pathway inhibitor currently in clinical trials, suppresses DP103 expression and Wnt/β-catenin signaling, reducing TNBC cell viability and mammosphere formation without affecting normal epithelial cells...Collectively, our findings establish DP103 as a key regulator of Wnt-driven oncogenesis in TNBC and highlight its dual role in promoting CSC traits and therapeutic resistance. These insights position DP103 as a potential biomarker and therapeutic target to disrupt sustained Wnt signaling in TNBC, offering new avenues for precision intervention in this challenging breast cancer subtype.

Moreover, alterations in FOXM1 expression, either via overexpression or knockdown, did not alter NOB-induced miR-342-3p levels but markedly impacted NOB's suppression of self-renewal in both HeLa cells and derived CCSLCs. Thus, NOB inhibits self-renewal by enhancing miR-342-3p levels and diminishing FOXM1 levels in CC cells and derived CCSLCs.

Narghile smoke induced histological and molecular changes in the tongue and tracheal epithelium of mice, indicating a potential carcinogenic effect. Further in vitro, in vivo, and clinical investigations are warranted to validate these biomarkers and better elucidate the biological effects of narghile smoke exposure.

Markers of pluripotency and self-renewal of embryonic stem cells are expressed until mid-pregnancy, contributing to the adult adrenal stem cell niche. They are absent postnatally but are expressed in a subset of ACT. Specifically, pS45P beta-catenin-mutated ACTs express more NANOG. Increased OCT4 expression in pACT is associated with worse prognosis, and inhibiting the Wnt/beta-catenin pathway in these cells impairs NANOG expression.

The stemness transcriptional response was not uniform with increased OCT4 expression, but unchanged SOX2 and NANOG levels. These findings warrant further translational investigation, including comprehensive reactive-species profiling.

Splenic hamartoma with bizarre stromal cells is exceedingly rare, with only seven cases previously reported in the English literature. These atypical cells can mimic malignancy, posing a diagnostic challenge. We report this case to highlight these diagnostic pitfalls alongside a literature review.

Chronic HG promoted stem-like and radioresistant phenotypes in NSCLC cells. Prolonged HBO exposure for 4 weeks attenuated these effects and was associated with reduced HIF-1α, SOX2, and OCT4 expression, supporting HBO as a potential preclinical adjunct strategy for mitigating HG-associated therapeutic resistance.

Consistent with previous reports of increased senescence, our findings demonstrate significant downregulation of stemness-related genes (NANOG, OCT4) in MSCs from newly diagnosed, untreated patients with MM. This concurrent dysregulation of stemness and increased senescent phenotype may contribute to the pathogenicity of the tumor microenvironment and represents a potential target for therapeutic intervention.

The stability of BACH1 mRNA following actinomycin D (ActD) treatment was analyzed after YTHDC1 silencing...Collectively, YTHDC1 regulates BACH1 expression in an m6A-dependent mechanism, contributing to TNBC progression. Implications: Our findings provide a rationale for further investigation of the YTHDC1/BACH1 axis as a potential therapeutic target in TNBC.

Taken together, the hMPEC and mice in situ models were constructed by our team for the first time, wherein DHA@ZIF-8 exhibits potent chemotherapeutic efficacy in these models. DHA@ZIF-8 facilitates M1 polarization of macrophages through the depression of the OCT4/NF-κB/M-CSF signaling pathway to enhance immunotherapeutic efficacy simultaneously, which provides a critical basis for DHA and bionanomaterial application in MPE treatment in the future.

This OSK-induced priming overcomes the cytokinesis barrier in proliferating CMs both in vitro and in vivo, yielding mononuclear CMs with high proliferative potential and ultimately enhancing cardiac repair after MI. Our findings reveal that OSK promotes regeneration primarily by priming dedifferentiation and overcoming cytokinesis bottlenecks, rather than by directly inducing CM S-phase entry, and establish OSK as a novel, safer reprogramming-based strategy for the treatment of MI.