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Lu-ming Yao

Researcher at Xiamen University

Publications -  5
Citations -  395

Lu-ming Yao is an academic researcher from Xiamen University. The author has contributed to research in topics: Apoptosis & Autophagy. The author has an hindex of 5, co-authored 5 publications receiving 285 citations.

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Orphan nuclear receptor TR3 acts in autophagic cell death via mitochondrial signaling pathway

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.
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Ectosomal PKM2 Promotes HCC by Inducing Macrophage Differentiation and Remodeling the Tumor Microenvironment

TL;DR: It is demonstrated that hepatocellular carcinoma (HCC)-derived ectosomes remodel the tumor microenvironment to facilitate HCC progression in an ectosomal PKM2-dependent manner and is revealed as a potential diagnostic marker for HCC.
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The orphan receptor TR3 suppresses intestinal tumorigenesis in mice by downregulating Wnt signalling

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.
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Orphan receptor TR3 participates in cisplatin-induced apoptosis via Chk2 phosphorylation to repress intestinal tumorigenesis

TL;DR: It is demonstrated that cisplatin effectively induces orphan nuclear receptor TR3 phosphorylation by activating Chk2 kinase activity and promoting cross talk between these two proteins, thereby contributing to the repression of intestinal tumorigenesis via apoptosis.
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Flightless-I Blocks p62-Mediated Recognition of LC3 to Impede Selective Autophagy and Promote Breast Cancer Progression.

TL;DR: It is reported that Flightless-I, a novel p62-interacting protein, promotes breast cancer progression by impeding selective autophagy by interacting with p62 to block its recognition of LC3, leading to tumorigenesis in breast cancer.