JNK acts as a molecular brake of the CDC73 positive feedback loop to modulate osteosarcoma malignant progression via UBR5.

Mechanistic Role of eIF4E in the Hallmarks of Cancer: A Translational Control Perspective.

Cancer progression is driven by coordinated dysregulation of signaling and gene-expression programs that sustain multiple hallmarks of malignancy. Eukaryotic initiation factor 4E (eIF4E) has emerged as an important determinant of this translational reprogramming by preferentially enhancing the synthesis of proteins tha...

The RBP2–BECN1–VEGFA axis orchestrates a self-amplifying circuit to drive malignant progression in gastric carcinoma

Objective Gastric carcinoma (GC) is a leading cause of cancer-related mortality, often driven by epigenetic dysregulation. This study investigates the role of Retinoblastoma-binding protein 2 (RBP2), a chromatin-associated transcriptional regulator frequently overexpressed in GC. We specifically focus on elucidating ho...

UBR5-KDM5A axis rewires redox metabolism to confer cisplatin resistance in triple-negative breast cancer via the cAMP-PKA-SIRT3 cascade.

Triple-negative breast cancer (TNBC) lacks actionable therapeutic targets and remains highly dependent on cytotoxic chemotherapy, yet the rapid emergence of cisplatin resistance severely limits clinical benefits. The molecular mechanisms underlying this resistance and effective combination strategies remain incompletel...

ACTB promotes ESCC progression by regulating the AKT-mTOR signaling pathway through an m6A-dependent mechanism.

Esophageal squamous cell carcinoma (ESCC) is a highly aggressive malignancy with poor prognosis, and the upstream regulatory mechanisms driving oncogenic signaling remain insufficiently defined. In this study, we identify a previously unrecognized nuclear function of the cytoskeletal protein ACTB in promoting ESCC prog...

Targeting FEN1 disrupts EIF4A3-mediated MUC1-C autoregulation: a novel strategy to suppress lung adenocarcinoma progression

The FEN1/EIF4A3/MUC1-C axis is established as a novel mechanism driving LUAD progression by concurrently regulating intrinsic malignancy and extrinsic immune evasion, presenting FEN1 targeting as a promising dual-hit therapeutic strategy.

Cell-cycle-driven noncanonical ubiquitination of METTL14 orchestrates RNA methylation.