Microenvironment responsive nanoplatform for targeted removal of cholesterol and reshaping inflammatory microenvironment in atherosclerotic plaques.

The microenvironment of atherosclerotic plaques features abundant cholesterol crystals (CCs), reactive oxygen species (ROS), and pro-inflammatory M1 macrophages, leading to the progression and mortality of atherosclerotic cardiovascular disease (ASCVD). Targeted removal of CCs and scavenging of ROS are crucial for treatment of ASCVD. In this study, an intelligent nanoformulation consisting of epigallocatechin gallate (EGCG), cysteine (Cys), ursodeoxycholic acid (UDCA) and VHPK (Valine-Histidine-Proline-Lysine)-Lipo, was designed to precisely target and remodel the inflammatory microenvironment of atherosclerotic plaques.

Cholesterol Targeted Catalytic Hydrogel Fueled by Tumor Debris can Enhance Microwave Ablation Therapy and Anti-Tumor Immune Response.

The immunosuppressive residual tumor microenvironment (IRTM) is a key factor in the high recurrence and metastasis rates of hepatocellular carcinoma (HCC) after microwave ablation (MWA). Cholesterol-rich tumor fragments significantly contribute to IRTM deterioration. This study developed a cholesterol-targeted catalytic hydrogel, DA-COD-OD-HCS, to enhance the synergy between MWA and immune checkpoint inhibitors (ICIs) for HCC treatment.

Corrigendum to "A novel FGFR1 inhibitor CYY292 suppresses tumor progression, invasion, and metastasis of glioblastoma by inhibiting the Akt/GSK3β/snail signaling axis" [Genes & Diseases 11 (2024) 479-494].

[This corrects the article DOI: 10.1016/j.gendis.

Synthesis of 9-Cinnamyl-9-purine Derivatives as Novel TLR4/MyD88/NF-κB Pathway Inhibitors for Anti-inflammatory Effects.

The novel 9-cinnamyl-9-purine skeleton, inspired by resveratrol and curcumin, was developed to avoid a pan-assay interference compound (PAINS) related to invalid metabolic pancreas activity (IMPS). It replaced the phenol group with purine analogues, the building blocks of DNA and RNA. Alterations to the hydroxyl group in the cinnamyl group, such as H, Me, or F substitutions, were made to impede its oxidation to a PAINS-associated quinone.

A novel FGFR1 inhibitor CYY292 suppresses tumor progression, invasion, and metastasis of glioblastoma by inhibiting the Akt/GSK3β/snail signaling axis.

Glioblastoma (GBM) is a malignant brain tumor that grows quickly, spreads widely, and is resistant to treatment. Fibroblast growth factor receptor (FGFR)1 is a receptor tyrosine kinase that regulates cellular processes, including proliferation, survival, migration, and differentiation. FGFR1 was predominantly expressed in GBM tissues, and FGFR1 expression was negatively correlated with overall survival.

The Effects of Triterpenoid Saponins from the Seeds of on Adipocyte Differentiation and Mature Adipocyte Inflammation.

Obesity is a medical condition in which abnormal or excessive fat accumulates to an extent that is associated with various diseases. In our ongoing research to figure out natural products with anti-obesity effects, a phytochemical investigation of the EtOH extract of the seeds of was carried out, which resulted in the isolation of two major triterpenoid saponins: gypsogenin 3---d-galactopyranosyl(1→2)-[-l-rhamnopyranosyl (1→3)]--d-glucuronopyranoside () and quillaic acid 3---d-galactopyranosyl(1→2)-[-l-rhamnopyranosyl(1→3)]--d-glucuronopyranoside (). Then, the effects of the isolated triterpenoid saponins ( and ) on adipocyte differentiation were evaluated, and it was demonstrated that the isolated saponin () showed inhibitory effects on adipogenesis.

A potent CBP/p300-Snail interaction inhibitor suppresses tumor growth and metastasis in wild-type p53-expressing cancer.

The zinc finger transcription factor Snail is aberrantly activated in many human cancers and associated with poor prognosis. Therefore, targeting Snail is expected to exert therapeutic benefit in patients with cancer. However, Snail has traditionally been considered "undruggable," and no effective pharmacological inhibitors have been identified.

A ZEB1/p53 signaling axis in stromal fibroblasts promotes mammary epithelial tumours.

Accumulating evidence indicates that the zinc-finger transcription factor ZEB1 is predominantly expressed in the stroma of several tumours. However, the role of stromal ZEB1 in tumour progression remains unexplored. In this study, while interrogating human databases, we uncover a remarkable decrease in relapse-free survival of breast cancer patients expressing high ZEB1 levels in the stroma.