Format

Send to

Choose Destination
Adv Exp Med Biol. 2019;1167:113-127. doi: 10.1007/978-3-030-23629-8_7.

Autophagy and Tumorigenesis in Drosophila.

Author information

1
Center for Cancer Cell Reprogramming (CanCell), Institute for Clinical Medicine, The Medical Faculty, University of Oslo, Oslo, Norway.
2
Department of Molecular Cell Biology, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway.
3
Center for Cancer Cell Reprogramming (CanCell), Institute for Clinical Medicine, The Medical Faculty, University of Oslo, Oslo, Norway. t.e.rusten@medisin.uio.no.
4
Department of Molecular Cell Biology, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway. t.e.rusten@medisin.uio.no.

Abstract

The resurgence of Drosophila as a recognized model for carcinogenesis has contributed greatly to our conceptual advance and mechanistic understanding of tumor growth in vivo. With its powerful genetics, Drosophila has emerged as a prime model organism to study cell biology and physiological functions of autophagy. This has enabled exploration of the contributions of autophagy in several tumor models. Here we review the literature of autophagy related to tumorigenesis in Drosophila. Functional analysis of core autophagy components does not provide proof for a classical tumor suppression role for autophagy alone. Autophagy both serve to suppress or support tumor growth. These effects are context-specific, depending on cell type and oncogenic or tumor suppressive lesion. Future delineation of how autophagy impinges on tumorigenesis will demand to untangle in detail, the regulation and flux of autophagy in the respective tumor models. The downstream tumor-regulative roles of autophagy through organelle homeostasis, metabolism, selective autophagy or alternative mechanisms remain largely unexplored.

KEYWORDS:

Atg; Autophagy; Keap1; LKB1; Mitochondria; Myc; N; NRF2; Notch; P62; PERK; PI3K; ROS; Raf; Scribble; Stem cell; TOR; Tumor; Upd; Uvrag; Yorkie; ras; scrib; vps34; yki

PMID:
31520352
DOI:
10.1007/978-3-030-23629-8_7
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Springer
Loading ...
Support Center