Receptor-interacting protein kinase 1 is a key mediator in TLR3 ligand and Smac mimetic-induced cell death and suppresses TLR3 ligand-promoted invasion in cholangiocarcinoma

Receptor-interacting protein kinase 1 is a key mediator in TLR3 ligand and Smac mimetic-induced cell death and suppresses TLR3 ligand-promoted invasion in cholangiocarcinoma

      Cholangiocarcinoma (CCA) is a cancer of the bile duct with no effective therapy. This study explores the potential of inducing ‘apoptosis’ and ‘necroptosis’, a form of cell death, as a new effective therapeutic strategy for the treatment of CCA patients. Here, the combination treatment with a Toll-like receptor 3 (TLR-3) ligand, and a smac mimetic, synergistically induced CCA cell death by apoptosis and necroptosis, and this killing is dependent on Receptor-interacting protein kinase 1 (RIPK1). Therefore, therapeutic targeting TLR3 by TLR3 ligands in combination with Smac mimetic could bring a new, effective therapeutic concept for the treatment of CCA patients.

 

Reference

Lomphithak T, Choksi S, Mutirangura A, Tohtong R, Tencomnao T, Usubuchi H, Unno M, Sasano H and Jitkaew S. Receptor-interacting protein kinase 1 is a key mediator in TLR3 ligand and Smac mimetic-induced cell death and suppresses TLR3 ligand-promoted invasion in cholangiocarcinoma. Cell Commun Signal. 2020; Oct 9;18(1):161. doi: 10.1186/s12964-020-00661-3.PMID: 33036630

BMCDOI: 10.1186/s12964-020-00661-3

 

Relevant SDGs
SDGs_Goal-3
BC investigator
Assoc. Prof. Rutaiwan Tohtong