Oral ruthenium-based PAD4 inhibitor modulates immunogenic cell death and neutrophil extracellular traps in triple-negative breast cancer.

Triple-negative breast cancer (TNBC) is a highly aggressive breast cancer subtype characterized by a poor prognosis and resistance to conventional therapies. Peptidylarginine deiminase 4 (PAD4), which catalyzes the conversion of arginine to citrulline, facilitating neutrophil extracellular trap (NET) formation and promoting tumor immune evasion, has been identified as a promising target for TNBC treatment. However, current PAD4 inhibitors have low bioavailability and inadequate stability.

Caffeic acid inhibits the tumorigenicity of triple-negative breast cancer cells through the FOXO1/FIS pathway.

Triple-negative breast cancer (TNBC) still one of the most challenging sub-type in breast cancer clinical. Caffeic acid (CA) derived from effective components of traditional Chinese herbal medicine has been show potential against TNBCs. Our research has found that CA can inhibit the proliferation of TNBC cells while also suppressing the size of cancer stem cell spheres.

The ruthenium complex assists in nuclear targeting and selective killing of tumor cells.

In clinical studies, the toxicity of platinum-based antitumor drugs limits their use. DNA is the most widely studied target of metal-based complexes. Thus, nuclear targeting and selective killing have become the purpose of ruthenium complex design.

Synthesis and Evaluation of a Paclitaxel-Binding Tripeptide Micelle for Lung Cancer Therapy.

A CCO-NalLeuVal (C10NLV) tripeptide was synthesized and explored as a carrier for paclitaxel (TAX) delivery. Five types of TAX-loaded micelles were produced by loading TAX with different doses of C10NLV. 3-(4,5-Dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay showed that TAX-loaded micelles dramatically reduced TAX IC values of TAX-resistant A549 (A549/TAX) and Lewis lung carcinoma (LLC) cells in a C10NLV-dose-dependent manner, with micelles 4 and 5 exhibited comparable inhibitory effects on A549/TAX proliferation.