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Genome-wide expression patterns associated with oncogenesis and sarcomatous transdifferentation of cholangiocarcinoma
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Genome-wide expression patterns associated with oncogenesis and sarcomatous transdifferentation of cholangiocarcinoma
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Targeting Oncogene-Induced Autophagy: A New Approach in Cancer Therapy?
Autophagy is a tightly controlled self-degradation process utilised by cells to sustain cellular homeostasis and to support cell survival in response to metabolic stress and starvation. Thus, autophagy plays a critical role in promoting cell integrity and maintaining proper function of cellular processes. Defects in autophagy, however, can have drastic implications in human health and diseases, including cancer. Described as a double-edged sword in the context of cancer, autophagy can act as both suppressor and facilitator of tumorigenesis. As such, defining the precise role of autophagy in a multistep event like cancer progression can be complex. Recent findings have implicated a role for components of the autophagy pathway in oncogene-mediated cell transformation, tumour growth, and survival. Notably, aggressive cancers driven by Ras oncoproteins rely on autophagy to sustain a reprogrammed mitochondrial metabolic signature and evade cell death. In this review, we summarize our current understanding of the role of oncogene-induced autophagy in cancer progression and discuss how modulators of autophagic responses can bring about therapeutic benefit and eradication of a subset of cancers that are addicted to this ancient recycling machinery. 1. Introduction Almost two decades ago, the Ohsumi laboratory first discovered and characterized the autophagy-related (ATG) genes in yeast [1, 2]. Since then, researchers around the world work relentlessly to unravel the biology of autophagy and its roles in a variety of human diseases. Autophagy can be broadly categorized into macroautophagy, microautophagy, and chaperone-mediated autophagy. Macroautophagy (hereafter autophagy) is a tightly regulated catabolic mechanism in the cell. It involves the sequestration of dysfunctional cytoplasmic constituents, ranging from misfolded proteins, proteoglycans and damaged organelles into double membrane vesicles, known as the autophagosomes. These autophagic vesicles eventually fuse with lysosomes, within which the dysfunctional cytoplasmic cargoes are degraded. This self-cannibalisation process in the cell appears to play a crucial role in supporting the bioenergetics and biosynthetic programs in response to nutrient deprivation and metabolic duress [3]. Under optimal growth conditions of a normal cell, the autophagic activity is kept in a minimal or basal state. Such basal autophagy is important for maintaining intracellular protein homeostasis and preservation of cellular integrity, through effective clearance of protein aggregates and damaged organelles. Under
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