Year: 2020
Type: editorial
Abstract: 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.
Source: Autophagy
Authors: Timothy Marsh, Jayanta Debnath
Language: English
Subfield: Epidemiology
Field: Medicine
Domain: Health Sciences
Open Access status: bronze
Awards: Stromal Fibroblast Autophagy In Tumor Progression and Desmoplasia, Autophagy as a microenvironmental regulator of tumorigenesis and resistance, Autophagy restricts breast cancer metastasis, Deciphering Autophagy-Dependent Secretion In Cancer Via Proximity-Based Biotinylation, Eliminating Late Recurrence to Eradicate Breast Cancer, G9000087205, Autophagy and Pro-metastatic Differentiation
OpenAlex ID: W3014263880