The force awakens: metastatic dormant cancer cells

Park, So‐Yeon; Nam, Jeong‐Seok

doi:10.1038/s12276-020-0423-z

Cited by 146 publications

(116 citation statements)

References 97 publications

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“…Signals responsible for triggering tumor outgrowth and colonization of secondary organs remain unknown, the participation of ECM components and aspects of tumor microenvironments likely play essential roles. Dormant cells are characterized by a reversible growth arrest in G 0 -G 1 cell cycle phases, reduced metabolism and a stem-cell-like phenotype ( 138 , 139 ). To survive to this stage, dormant cells activate autophagy.…”

Section: The Interplay Of Autophagy and Metastasismentioning

confidence: 99%

The Double-Edge Sword of Autophagy in Cancer: From Tumor Suppression to Pro-tumor Activity

et al. 2020

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During tumorigenesis, cancer cells are exposed to a wide variety of intrinsic and extrinsic stresses that challenge homeostasis and growth. Cancer cells display activation of distinct mechanisms for adaptation and growth even in the presence of stress. Autophagy is a catabolic mechanism that aides in the degradation of damaged intracellular material and metabolite recycling. This activity helps meet metabolic needs during nutrient deprivation, genotoxic stress, growth factor withdrawal and hypoxia. However, autophagy plays a paradoxical role in tumorigenesis, depending on the stage of tumor development. Early in tumorigenesis, autophagy is a tumor suppressor via degradation of potentially oncogenic molecules. However, in advanced stages, autophagy promotes the survival of tumor cells by ameliorating stress in the microenvironment. These roles of autophagy are intricate due to their interconnection with other distinct cellular pathways. In this review, we present a broad view of the participation of autophagy in distinct phases of tumor development. Moreover, autophagy participation in important cellular processes such as cell death, metabolic reprogramming, metastasis, immune evasion and treatment resistance that all contribute to tumor development, is reviewed. Finally, the contribution of the hypoxic and nutrient deficient tumor microenvironment in regulation of autophagy and these hallmarks for the development of more aggressive tumors is discussed.

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Section: The Interplay Of Autophagy and Metastasismentioning

confidence: 99%

The Double-Edge Sword of Autophagy in Cancer: From Tumor Suppression to Pro-tumor Activity

et al. 2020

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“…Furthermore, cancer cells can also exploit neuronal signaling pathways for growth and adaptation [ 20 ]. Cancer dormancy is an arrest phase that can occur after invasion into secondary sites and in some cancer survivors, dormant cells result in relapse long after the removal of the primary tumor [ 20 , 34 ]. The subsequent reactivation is governed by self-renewal pathways (e.g., Wnt, Hedgehog and Notch) and cells exhibit increased levels of stem cell associated genes [ 35 ].…”

Section: The Metastatic Cascadementioning

confidence: 99%

Obesity and Cancer Metastasis: Molecular and Translational Perspectives

Annett

Moore

Robson

2020

Cancers

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Obesity is a modern health problem that has reached pandemic proportions. It is an established risk factor for carcinogenesis, however, evidence for the contribution of adipose tissue to the metastatic behavior of tumors is also mounting. Over 90% of cancer mortality is attributed to metastasis and metastatic tumor cells must communicate with their microenvironment for survival. Many of the characteristics observed in obese adipose tissue strongly mirror the tumor microenvironment. Thus in the case of prostate, pancreatic and breast cancer and esophageal adenocarcinoma, which are all located in close anatomical proximity to an adipose tissue depot, the adjacent fat provides an ideal microenvironment to enhance tumor growth, progression and metastasis. Adipocytes provide adipokines, fatty acids and other soluble factors to tumor cells whilst immune cells infiltrate the tumor microenvironment. In addition, there are emerging studies on the role of the extracellular vesicles secreted from adipose tissue, and the extracellular matrix itself, as drivers of obesity-induced metastasis. In the present review, we discuss the major mechanisms responsible for the obesity–metastatic link. Furthermore, understanding these complex mechanisms will provide novel therapies to halt the tumor–adipose tissue crosstalk with the ultimate aim of inhibiting tumor progression and metastatic growth.

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“…While discussing the crosstalk between cellular redox metabolism and pathways that promote or regulate cell cycle progression, particularly SASP acquisition, it would be prudent and appropriate to also discuss this in the context of “tumor dormancy” 90 . Tumor dormancy might be viewed as a phenomenon similar to dormant viruses such as the herpes simplex virus and (HSV1&2), whereby a reservoir stays “cold” only to be reactivated upon a stress stimulus.…”

Section: Cellular Redox State Senescence and Carcinogenesismentioning

confidence: 99%

Cellular senescence: Silent operator and therapeutic target in cancer

et al. 2021

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The process of carcinogenesis and its progression involves an intricate interplay between a number of signaling networks, metabolic pathways and the microenvironment. These include an alteration in the cellular redox metabolism and deregulation of cell cycle checkpoints. Similar to the dichotomy of redox signaling in cancer cell fate and state determination, a diverging effect of an irreversible cell cycle arrest or senescence on carcinogenesis has been demonstrated. In this regard, while overwhelming oxidative stress has a damaging effect on tissue architecture and organ function and promotes death execution, a mild “pro‐oxidant” environment is conducive for cell proliferation, growth and survival. Similarly, cellular senescence has been shown to elicit both a tumor suppressor and an oncogenic effect in a context‐dependent manner. Notably, there appears to be a crosstalk between these two critical regulators of cell fate and state, particularly from the standpoint of the divergent effects on processes that promote or abate carcinogenesis. This review aims to provide an overview of these overarching themes and attempts to highlight critical intersection nodes, which are emerging as potential diagnostic and/or therapeutic targets for novel anticancer strategies.

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The force awakens: metastatic dormant cancer cells

Cited by 146 publications

References 97 publications

The Double-Edge Sword of Autophagy in Cancer: From Tumor Suppression to Pro-tumor Activity

The Double-Edge Sword of Autophagy in Cancer: From Tumor Suppression to Pro-tumor Activity

Obesity and Cancer Metastasis: Molecular and Translational Perspectives

Cellular senescence: Silent operator and therapeutic target in cancer

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