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Autophagy in cancer: a complex relationship.

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TLDR
This review will explore the connections between autophagy and cancer, which are tumor- and context-dependent and include the tumor microenvironment, and highlight the importance of tumor compartment-specific autophagic in both cancer aggressiveness and treatment.
Abstract
Macroautophagy is the process by which cells package and degrade cytosolic components, and recycle the breakdown products for future use. Since its initial description by Christian de Duve in the 1960s, significant progress has been made in understanding the mechanisms that underlie this vital cellular process and its specificity. Furthermore, macroautophagy is linked to pathologic conditions such as cancer and is being studied as a therapeutic target. In this review, we will explore the connections between autophagy and cancer, which are tumor- and context-dependent and include the tumor microenvironment. We will highlight the importance of tumor compartment-specific autophagy in both cancer aggressiveness and treatment.

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Citations
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Journal ArticleDOI

Tanshinone I attenuates the malignant biological properties of ovarian cancer by inducing apoptosis and autophagy via the inactivation of PI3K/AKT/mTOR pathway

TL;DR: This study aimed to access the therapy effect of Tan‐Ⅰ and the underlying mechanisms by which Tan‐ Ⅰ regulates apoptosis and autophagy in ovarian cancer.
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Autophagic flux disruption contributes to Ganoderma lucidum polysaccharide-induced apoptosis in human colorectal cancer cells via MAPK/ERK activation.

TL;DR: It is demonstrated that GLP-induced autophagosome accumulation and apoptosis is mediated via MAPK/ERK activation, and GLP inhibited tumor growth and also inhibited autophagic flux in vivo.
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Starvation-induced autophagy promotes the invasion and migration of human bladder cancer cells via TGF-β1/Smad3-mediated epithelial-mesenchymal transition activation.

TL;DR: It is suggested that autophagy promotes the invasion and migration of bladder cancer cells by inducing EMT through the TGF‐β1/Smad3 signaling pathway and can form a positive feedback loop to synergistically promote invasion and Migration.
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p62-mediated Selective Autophagy Endows Virus-Transformed Cells With Insusceptibility to DNA Damage Under Oxidative Stress

TL;DR: Evidence is provided that considerable levels of p62-mediated selective autophagy are spontaneously induced, and correlate with ROS-Keap1-NRF2 pathway activity, in virus-transformed cells, and a novel insight into virus-mediated oncogenesis is provided.
Journal ArticleDOI

Anticancer Effects of Green Tea and the Underlying Molecular Mechanisms in Bladder Cancer.

TL;DR: The potential usefulness of green Tea as an antibladder cancer agent and the future direction of green tea-based treatment strategies for patients with bladder cancer are discussed.
References
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Journal ArticleDOI

AMPK and mTOR regulate autophagy through direct phosphorylation of Ulk1

TL;DR: A molecular mechanism for regulation of the mammalian autophagy-initiating kinase Ulk1, a homologue of yeast ATG1, is demonstrated and a signalling mechanism for UlK1 regulation and autophagic induction in response to nutrient signalling is revealed.
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Bcl-2 antiapoptotic proteins inhibit Beclin 1-dependent autophagy.

TL;DR: Bcl-2 not only functions as an antiapoptotic protein, but also as an antiautophagy protein via its inhibitory interaction with Beclin 1, which may help maintain autophagy at levels that are compatible with cell survival, rather than cell death.
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AMPK phosphorylation of raptor mediates a metabolic checkpoint.

TL;DR: AMPK directly phosphorylates the mTOR binding partner raptor on two well-conserved serine residues, and this phosphorylation induces 14-3-3 binding to raptor, uncovering a conserved effector of AMPK that mediates its role as a metabolic checkpoint coordinating cell growth with energy status.
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Self-eating and self-killing: crosstalk between autophagy and apoptosis

TL;DR: The functional relationship between apoptosis and autophagy is complex in the sense that, under certain circumstances,autophagy constitutes a stress adaptation that avoids cell death (and suppresses apoptosis), whereas in other cellular settings, it constitutes an alternative cell-death pathway.
Journal ArticleDOI

Induction of autophagy and inhibition of tumorigenesis by beclin 1.

TL;DR: It is shown that beclin 1 is a mammalian autophagy gene that can inhibit tumorigenesis and is expressed at decreased levels in human breast carcinoma, suggesting that decreased expression of Autophagy proteins may contribute to the development or progression of breast and other human malignancies.
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