Role of Autophagy in Breast Cancer Development and Progression: Opposite Sides of the Same Coin.

Abstract:

:The term "autophagy", which means "self (auto) - eating (phagy)", describes a catabolic process that is evolutionarially conserved among all eukaryotes. Although autophagy is mainly accepted as a cell survival mechanism, it also modulates the process known as "type II cell death". AKT/mTOR pathway is an upstream activator of autophagy and it is tightly regulated by the ATG (autophagy-related genes) signaling cascade. In addition, wide ranging cell signaling pathways and non-coding RNAs played essential roles in the control of autophagy. Autophagy is closely related to pathological processes such as neurodegenerative diseases and cancer as well as physiological conditions. After the Nobel Prize in Physiology or Medicine 2016 was awarded to Yoshinori Ohsumi "for his discoveries of mechanisms for autophagy", there was an explosion in the field of autophagy and molecular biologists started to pay considerable attention to the mechanistic insights related to autophagy in different diseases. Since autophagy behaved dualistically, both as a cell death and a cell survival mechanism, it opened new horizons for a deeper analysis of cell type and context dependent behavior of autophagy in different types of cancers. There are numerous studies showing that the induction of autophagy mechanism will promote survival of cancer cells. Since autophagy is mainly a mechanism to keep the cells alive, it may protect breast cancer cells against stress conditions such as starvation and hypoxia. For these reasons, autophagy was noted to be instrumental in metastasis and drug resistance. In this chapter we have emphasized on role of role of autophagy in breast cancer. Additionally we have partitioned this chapter into exciting role of microRNAs in modulation of autophagy in breast cancer. We have also comprehensively summarized how TRAIL-mediated signaling and autophagy operated in breast cancer cells.

journal_name

Adv Exp Med Biol

authors

Romero MA,Bayraktar Ekmekcigil O,Bagca BG,Avci CB,Sabitaliyevich UY,Zhenisovna TG,Aras A,Farooqi AA

doi

10.1007/978-3-030-20301-6_5

subject

Has Abstract

pub_date

2019-01-01 00:00:00

pages

65-73

eissn

0065-2598

issn

2214-8019

journal_volume

1152

pub_type

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