The CTLH Complex in Cancer Cell Plasticity.
Nickelas HuffmanDario PalmieriVincenzo CoppolaPublished in: Journal of oncology (2019)
Cancer cell plasticity is the ability of cancer cells to intermittently morph into different fittest phenotypic states. Due to the intrinsic capacity to change their composition and interactions, protein macromolecular complexes are the ideal instruments for transient transformation. This review focuses on a poorly studied mammalian macromolecular complex called the CTLH (carboxy-terminal to LisH) complex. Currently, this macrostructure includes 11 known members (ARMC8, GID4, GID8, MAEA, MKLN1, RMND5A, RMND5B, RANBP9, RANBP10, WDR26, and YPEL5) and it has been shown to have E3-ligase enzymatic activity. CTLH proteins have been linked to all fundamental biological processes including proliferation, survival, programmed cell death, cell adhesion, and migration. At molecular level, the complex seems to interact and intertwine with key signaling pathways such as the PI3-kinase, WNT, TGFβ, and NFκB, which are key to cancer cell plasticity. As a whole, the CTLH complex is overexpressed in the most prevalent types of cancer and may hold the key to unlock many of the biological secrets that allow cancer cells to thrive in harsh conditions and resist antineoplastic therapy.
Keyphrases
- signaling pathway
- cell adhesion
- stem cells
- cell proliferation
- oxidative stress
- epithelial mesenchymal transition
- pi k akt
- immune response
- single molecule
- inflammatory response
- hydrogen peroxide
- amino acid
- mesenchymal stem cells
- patient reported outcomes
- endoplasmic reticulum stress
- smoking cessation
- subarachnoid hemorrhage