Autophagy suppresses breast cancer metastasis by degrading NBR1

Macroautophagy/autophagy plays complex, context-dependent roles in cancer. How autophagy governs the emergence of metastatic disease has been incompletely understood. We recently uncovered that genetic autophagy inhibition strongly attenuates primary tumor growth in mammary cancer models, yet parado...

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Bibliographic Details
Published inAutophagy Vol. 16; no. 6; pp. 1164 - 1165
Main Authors Marsh, Timothy, Debnath, Jayanta
Format Journal Article
LanguageEnglish
Published United States Taylor & Francis 02.06.2020
Subjects
Autophagic Punctum
Autophagy
Breast Neoplasms
Carrier Proteins
chloroquine
Humans
Intracellular Signaling Peptides and Proteins
keratin14
Macroautophagy
metastasis
NBR1
rubicon
TP63
chloroquine
keratin14
metastasis
NBR1
rubicon
Autophagy
TP63
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Summary:Macroautophagy/autophagy plays complex, context-dependent roles in cancer. How autophagy governs the emergence of metastatic disease has been incompletely understood. We recently uncovered that genetic autophagy inhibition strongly attenuates primary tumor growth in mammary cancer models, yet paradoxically promotes spontaneous metastasis to the lung and enables the outgrowth of disseminated tumor cells (DTCs) into overt macro-metastases. Furthermore, at both primary and metastatic sites, genetic autophagy inhibition leads to the marked expansion of tumor cells exhibiting aggressive and pro-metastatic basal epithelial differentiation. These pro-metastatic effects of autophagy inhibition are due to the cytosolic accumulation of the autophagy cargo receptor NBR1 in autophagy-deficient tumor cells.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
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ISSN:1554-8627
1554-8635
DOI:10.1080/15548627.2020.1753001