Given its oncogenic potential, this study aimed to investigate the potential of SOX2 as a biomarker and evaluate the inhibitory effects of cordycepin (CD), a natural compound, on SOX2-driven oncogenic phenotypes in lung cancer...Moreover, overexpression of SOX2 promoted lung cancer cell growth, migration, and invasion, while CD, a natural product originally from the traditional Chinese medicine Cordyceps sinensis (BerK.), suppressed SOX2-mediated progression, including the growth, migration, and invasion of lung cancer. Taken together, these results implied that SOX2 is a potential biomarker for diagnostics, prognostics, and therapeutics for lung cancer, including LUAD and LUSC.

Our work uncovers a previously unrecognized PRKN-METTL3-CLDN2 signaling network that orchestrates colorectal tumorigenesis, providing a compelling rationale for developing METTL3-targeted therapies against CRC.

Our findings establish the ALKBH5/IGF2BP1-TRIM37-RBMX signaling axis as a pivotal driver of PDAC progression, highlighting the intersection of m6A modification, ubiquitin signaling, and metabolic reprogramming. These findings may provide potential therapeutic avenues for this intractable malignancy.

We have established the circ-ZBTB38/RALGAPB axis as a novel regulatory circuit in melanoma. Circ-ZBTB38 mediates RALGAPB post-translational degradation to hyperactivate Ral signaling. This work uncovers a new mechanism of circRNA-mediated regulation of enzyme activity (RalGAPs) in signaling crosstalk and highlights circ-ZBTB38 as a prognostic biomarker and therapeutic target for melanoma.

P4, N=150, Not yet recruiting, University of Miami

Here, we demonstrate that expression of DYRK1B - but not its closely related paralog DYRK1A - is upregulated by cytostatic drugs (Actinomycin D, Doxorubicin) in multiple cancer cell lines. In conclusion, our study identifies DYRK1B as an indirect p53 target that suppresses p53-mediated activation of RFX7. These findings suggest that pharmacological inhibition of DYRK1B may represent a therapeutic strategy to enhance RFX7 tumor suppressor function.

The review lists over 18 mushroom species (e.g., Ganoderma lucidum, Cordyceps, Phellinus) and 28 bioactive compounds (such as Ganoderic acid DM, Cordycepin, Hispidin) that affect autophagy, demonstrating efficacy against 15 cancer types, including colorectal, lung, breast, and liver cancers...The context-dependent effects of autophagy, along with the limited clinical evidence, present considerable challenges. Future clinical trials must focus on developing standardized extracts and personalized approaches to effectively translate this potential into clinical practice.

We induce a patient-derived xenograft model (KT-47) to develop blastemal predominance after chemotherapy and to become resistant to vincristine, actinomycin-D, and doxorubicin (VAD). These findings are validated in additional Wilms tumor models. Overall, resistance is associated with de-differentiation to a stem-like state and is driven by ABCB1 upregulation, suggesting that therapeutic strategies targeting chromatin regulation and drug efflux may be relevant in therapy-resistant Wilms tumor.

The interaction between SNRPA1 and METTL3 or IGF2BP2 was studied using RIP assay, dual-luciferase reporter assay, and actinomycin D assay, while the association of SNRPA1 with TWIST was determined through Co-IP assay and CHX assay...The METTL3/IGF2BP2-mediated m6A methylation modification of SNRPA1 binds to TWIST1 to promote NSCLC cell proliferation, migration, and invasion, ultimately leading to NSCLC progression. The online version contains supplementary material available at 10.1007/s10616-026-00924-w.

ARPC1B drives GC progression by stabilizing HK2 mRNA through IGF2BP3 binding, thereby potentiating glycolytic reprogramming to facilitate tumor growth and metastasis. Targeting the ARPC1B-IGF2BP3-HK2 axis may represent a novel therapeutic strategy for GC.

Mice exhibiting PTSD-like behaviour were treated with fluoxetine (FLU, 10 mg/kg), an antidepressant drug, and COR (10 and 50 mg/kg). COR demonstrated a dose-dependent response with 50 mg/kg showing consistent improvement in both behavioural and biochemical parameters. Overall, COR exhibited promising activity in this model and may serve as a potential natural therapeutic strategy to investigate for the management of PTSD in clinics.

US Food and Drug Administration-approved DNMT inhibitors, such as decitabine and azacitidine, and investigational agents including RX-3117 and SGI-1027 selectively suppressed the growth of VHL-deficient RCC cells. Further mechanistic analysis showed that KCNK3 reactivation triggers TNF-α, MAPK and apoptotic signaling pathways, contributing to the observed synthetic lethality. Collectively, these findings establish DNMT inhibition as a synthetic lethal strategy in VHL-deficient RCC and highlight a potential therapeutic vulnerability for personalized treatment approaches.