TRIM59 deficiency curtails breast cancer metastasis through SQSTM1-selective autophagic degradation of PDCD10. Academic Article

abstract

• Receptor-driven selective macroautophagy/autophagy delivers ubiquitinated targets for autophagosomal clearance to maintain metabolic homeostasis and orchestrate reparative inflammatory responses. Deregulated autophagy is linked to tumor progression, but the exact mechanisms of selective autophagy in the spatiotemporal control of cell polarity signaling components during cancer metastasis remain ill-defined. Our recent study has demonstrated that TRIM59, an E3 ligase upregulated in metastatic breast cancer, is required for cancer cell survival and metastasis. Genetic depletion of TRIM59 suppresses cancer metastasis by promoting RNFT1-induced K63 polyubiquitination and SQSTM1-directed autophagic degradation of PDCD10, thereby boosting ROCK (Rho associated coiled-coil containing protein kinase)-induced actomyosin contractility and enhancing CDH1-mediated adhesion formation.

authors

• Zhou, Yubin

published proceedings

• Autophagy

author list (cited authors)

• Tan, P., He, L., & Zhou, Y.

citation count

• 16

complete list of authors

• Tan, Peng||He, Lian||Zhou, Yubin

publication date

• January 2019

publisher

• Taylor & Francis  Publisher

published in

• Autophagy  Journal

keywords

• Actomyosin Contractility
• Apoptosis Regulatory Proteins
• Autophagy
• Breast Cancer
• Breast Neoplasms
• Cell Adhesion
• Cerebral Cavernous Malformation
• Humans
• Intracellular Signaling Peptides And Proteins
• Membrane Proteins
• Metalloproteins
• Metastasis
• Pdcd10
• Proto-Oncogene Proteins
• Rnft1
• Selective Autophagy
• Sequestosome-1 Protein
• Signal Transduction
• Trim59
• Tripartite Motif Proteins
• Ubiquitin-Protein Ligases
• Ubiquitination

Digital Object Identifier (DOI)

• 10.1080/15548627.2019.1569951

start page

• 747

end page

• 749

volume

• 15

issue

• 4

URL

• http://dx.doi.org/10.1080/15548627.2019.1569951