Li Li

TL;DR: It is discovered that melanoma, which is generally resistant to drug-induced apoptosis, can undergo autophagic cell death with the participation of orphan nuclear receptor TR3, and implicates a new approach to melanoma therapy through activation of a mitochondrial signaling pathway that integrates a nuclear receptor with autophagy for cell death.

TL;DR: It is shown that orphan nuclear receptor Nur77 (also known as TR3) can enhance resistance to lipopolysaccharide-induced sepsis in mice by inhibiting NF-κB activity and suppressing aberrant cytokine production.

TL;DR: C-DIMs such as DIM-C-pPhOH directly bind NR4A1 and are NR4 a1 antagonists in colon cancer cells, and their antineoplastic activity is due, in part, to their interactions with nuclear NR4a1.

TL;DR: TR3 is a negative regulator of Wnt signalling and thus significantly suppresses intestinal tumorigenesis in Apcmin/+ mice, and this inhibitory effect of TR3 may be paradoxically overcome through phosphorylation by GSK3β in clinical colorectal cancers.

TL;DR: These findings provide a new and viable therapeutic strategy for melanomas harboring NRAS mutations, and develop ZT-12-037-01 (1a) as a specific STK19-targeted inhibitor and showed that it effectively blocks oncogenic NRAS-driven melanocyte malignant transformation and melanoma growth in vitro and in vivo.