TRIM11, a direct target of miR-24-3p, promotes cell proliferation and inhibits apoptosis in colon cancer TRIM11, a direct target of miR-24-3p, promotes cell proliferation and inhibits apoptosis in colon cancer

Genetic polymorphisms of Wnt/β-catenin pathway genes are associated with the efficacy and toxicities of radiotherapy in patients with nasopharyngeal carcinoma Genetic polymorphisms of Wnt/β-catenin pathway genes are associated with the efficacy and toxicities of radiotherapy in patients with nasopharyngeal carcinoma

Galangin, a natural flavonoid product derived from the root of galangal, is emerging as a promising anticancer agent against multiple cancers. Yet, whether it also has antitumor effects on cholangiocarcinoma (CCA) and the underlying mechanism is still unknown. Herein, we demonstrate that galangin exhibits multiple antitumor effects on CCA cells including decreases cell viability; inhibits proliferation, migration, and invasion; and induces apoptosis. Moreover, those phenotypic changes are associated with downregulated microRNA‐21 (miR‐21) expression. To support, overexpression of miR‐21 blocks galangin‐mediated antisurvival and metastasis effects on CCA cells. Mechanically, galangin increases the expression of phosphatase and tensin homolog (PTEN), a direct target of miR‐21, resulting in decreased phosphorylation of AKT, a protein kinase which plays a critical role in controlling survival and apoptosis. In contrast, overexpression of miR‐21 abrogates galangin‐regulated PTEN expression and AKT phosphorylation. Taken together, these findings indicate that galangin inhibits CCA cell proliferation and metastasis and induces cell apoptosis through a miR‐21‐dependent manner, and galangin may provide a novel potential therapeutic adjuvant to treat CCA.

Renal cell carcinoma (RCC) is a common malignant tumor with metabolic reprogramming and immune evasion features. δ-Aminolevulinic acid dehydratase (ALAD), a key enzyme in heme biosynthesis, has been implicated in cancer progression and treatment outcomes, but its role in RCC remains unclear. This study integrated multi-omics datasets from TCGA, CPTAC, and GEO to analyze ALAD's expression, prognostic value, and functional implications in RCC. The results showed that ALAD expression is significantly downregulated in RCC tissues at both transcriptomic and proteomic levels, with low expression associated with advanced tumor stages, poor prognosis, and altered metabolic pathways. Functional enrichment and metabolic signature analyses revealed ALAD's association with metabolic processes and immune cell infiltration, particularly impacting CD8+ T cell-mediated immunity. Furthermore, ALAD expression correlated with sensitivity to specific anticancer drugs, suggesting potential therapeutic implications that required functional confirmation. Overall, this study suggestes that ALAD is a promising prognostic biomarker and therapeutic target in RCC, highlighting its role in modulating the tumor immune microenvironment and metabolic landscape. These findings highlight an association between ALAD and RCC progression, though experimental validation is needed to confirm causality.

Pulmonary fibrosis (PF) is a progressive and ultimately fatal lung disorder characterized by irreversible parenchymal scarring. Current therapeutic interventions are limited by suboptimal efficacy and significant adverse effects, highlighting a critical unmet need for the development of effective antioxidant therapeutic strategies. In this study, we engineered a novel nanotherapeutic platform composed of chondroitin sulfate (Chs)‐functionalized molybdenum disulfide nanosheets (CLM NSs) for targeted PF therapy. The system was synthesized through lipoic acid (LA)‐mediated conjunction of Chs to MoS ₂ nanosheets, significantly enhancing their physiological stability. CLM NSs utilize a CD44 receptor‐mediated targeting mechanism: initial pulmonary accumulation is achieved by attaching to circulating macrophages during the early inflammatory phase, followed by direct recognition of CD44 overexpressed on diseased alveolar epithelial cells in the late phase, enabling precise lesion‐specific accumulation. The nanosheets demonstrated robust broad‐spectrum antioxidant capacity, efficiently scavenging reactive oxygen/nitrogen species (ROS/RNS), restoring pulmonary redox homeostasis, and significantly inhibiting fibroblast activation and epithelial‐mesenchymal transition (EMT). In a bleomycin‐induced murine PF model, CLM NSs exerted significant therapeutic effects, markedly attenuating fibrotic progression, preserving alveolar architecture, and reducing pathological collagen deposition. Mechanistically, their therapeutic action involves inhibition of the critical ROS‐STAT1‐CXCL10 signaling axis, consequently suppressing macrophage recruitment and the inflammatory cascade. This nanoplatform, integrating efficient targeting, potent antioxidant activity, and excellent biocompatibility, represents a highly promising strategy for PF treatment.