Parallels between wound healing, epimorphic regeneration and solid tumors

Wong, Alan Y.; Whited, Jessica L.

doi:10.1242/dev.181636

Cited by 27 publications

(28 citation statements)

References 164 publications

(253 reference statements)

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“…Regenerative and tumorigenic cells have been recognized to have similar features, based on their proliferative character in functional organs. These assumptions are frequently based on comparison between one tissue type that can regenerate with another different cell type that forms a tumor (Milanovic et al, 2018;Oviedo and Beane, 2009;Sarig and Tzahor, 2017;Wong and Whited, 2020). The power of our approach relies on the examination of the same cell type, namely post-embryonic cardiomyocytes, which have been stimulated to enter the cell-cycle either by the regenerative or the oncogenic program.…”

Section: Discussionmentioning

confidence: 99%

“…None of these studies report incidents of tumors. One possible explanation is that regenerativecompetent cells might possess mechanisms that halt abnormal cell proliferation, preventing a neoplastic danger (Rojas-Muñoz et al, 2009;Stewart et al, 2013;Tanaka, 2016;Wong and Whited, 2020). How regenerating tissues are resistant to tumor formation in organisms with a high level of regeneration is not well understood.…”

Section: Discussionmentioning

confidence: 99%

“…The epimorphic regeneration reconstructs the damaged organ, whereas a tumor ruins the organ architecture. Whether the hyperplastic nature of regenerative-competent and tumorigenic cells shares other common cellular and molecular mechanisms is still being disputed (Charni et al, 2017;Milanovic et al, 2018;Oviedo and Beane, 2009;Pomerantz and Blau, 2013;Sarig and Tzahor, 2017;Stiehl and Marciniak-Czochra, 2017;Wong and Whited, 2020).…”

Section: Introductionmentioning

confidence: 99%

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Oncogene-induced cardiac neoplasia shares similar mechanisms with heart regeneration in zebrafish

Pfefferli

Bonvin

Robatel

et al. 2020

Preprint

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The human heart is a poorly regenerative organ and cardiac tumors are extremely rare. The zebrafish heart can restore its damaged myocardium through cardiomyocyte proliferation. Whether this endogenous capacity causes a susceptibility to neoplasia remains unknown. Here, we established a strategy to conditionally express the HRASG12V oncogene in zebrafish cardiomyocytes. The induction of this transgene in larvae or adult animals resulted in heart overgrowth with abnormal histology. The malformed ventricle displayed similar characteristics to the regenerative myocardium, such as enhanced cell-cycle entry, incomplete differentiation, reactivation of cardiac embryonic programs, expression of regeneration genes, oxidative metabolism changes, intramyocardial matrix remodeling and leucocyte recruitment. We found that oncogene-mediated cardiac tumorigenesis and cryoinjury-induced regeneration involve TOR signaling, as visualized by phosphorylation of its target ribosomal protein S6. The inhibition of TOR by rapamycin impaired regeneration and rescued from neoplasia. These findings demonstrate the existence of common mechanisms underlying the proliferative plasticity of zebrafish cardiomyocytes during advantageous organ restoration and detrimental tumorigenesis.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Oncogene-induced cardiac neoplasia shares similar mechanisms with heart regeneration in zebrafish

Pfefferli

Bonvin

Robatel

et al. 2020

Preprint

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“…During the next step, the tumor gains malignant properties. Enhanced angiogenesis, invasion, and metastasis facilitate tumor progression [ 62 ]. Literature reports indicate that alterations at the actin level may also be important in the process of DNA repair, chromatin remodeling, or activation of oncogenes, necessary in the initial stages of carcinogenesis [ 63 , 64 , 65 ].…”

Section: Actin and Abps In Carcinogenesismentioning

confidence: 99%

Involvement of Actin and Actin-Binding Proteins in Carcinogenesis

Izdebska

Zielińska

Hałas‐Wiśniewska

et al. 2020

Cells

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The actin cytoskeleton plays a crucial role in many cellular processes while its reorganization is important in maintaining cell homeostasis. However, in the case of cancer cells, actin and ABPs (actin-binding proteins) are involved in all stages of carcinogenesis. Literature has reported that ABPs such as SATB1 (special AT-rich binding protein 1), WASP (Wiskott-Aldrich syndrome protein), nesprin, and villin take part in the initial step of carcinogenesis by regulating oncogene expression. Additionally, changes in actin localization promote cell proliferation by inhibiting apoptosis (SATB1). In turn, migration and invasion of cancer cells are based on the formation of actin-rich protrusions (Arp2/3 complex, filamin A, fascin, α-actinin, and cofilin). Importantly, more and more scientists suggest that microfilaments together with the associated proteins mediate tumor vascularization. Hence, the presented article aims to summarize literature reports in the context of the potential role of actin and ABPs in all steps of carcinogenesis.

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“…The tumor microenvironment morphologically resembles a healing wound site [ 4 ], which is composed of multiple histological changes: extravascular clotting, inflammatory cell infiltration, angiogenesis, accumulation of activated fibroblasts, and synthesis of extracellular matrix (ECM) [ 4 , 5 ]. Activated fibroblasts in wound healing sites, display a contractile phenotype with enhanced expression of α-smooth muscle actin (α-SMA) and therefore are referred to as myofibroblasts.…”

Section: Introductionmentioning

confidence: 99%

Emergence of Cancer-Associated Fibroblasts as an Indispensable Cellular Player in Bone Metastasis Process

Mukaida

Zhang

Sasaki

2020

Cancers

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Bone metastasis is frequently complicated in patients with advanced solid cancers such as breast, prostate and lung cancers, and impairs patients’ quality of life and prognosis. At the first step of bone metastasis, cancer cells adhere to the endothelium in bone marrow and survive in a dormant state by utilizing hematopoietic niches present therein. Once a dormant stage is disturbed, cancer cells grow through the interaction with various bone marrow resident cells, particularly osteoclasts and osteoblasts. Consequently, osteoclast activation is a hallmark of bone metastasis. As a consequence, the drugs targeting osteoclast activation are frequently used to treat bone metastasis but are not effective to inhibit cancer cell growth in bone marrow. Thus, additional types of resident cells are presumed to contribute to cancer cell growth in bone metastasis sites. Cancer-associated fibroblasts (CAFs) are fibroblasts that accumulate in cancer tissues and can have diverse roles in cancer progression and metastasis. Given the presence of CAFs in bone metastasis sites, CAFs are emerging as an important cellular player in bone metastasis. Hence, in this review, we will discuss the potential roles of CAFs in tumor progression, particularly bone metastasis.

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Parallels between wound healing, epimorphic regeneration and solid tumors

Cited by 27 publications

References 164 publications

Oncogene-induced cardiac neoplasia shares similar mechanisms with heart regeneration in zebrafish

Oncogene-induced cardiac neoplasia shares similar mechanisms with heart regeneration in zebrafish

Involvement of Actin and Actin-Binding Proteins in Carcinogenesis

Emergence of Cancer-Associated Fibroblasts as an Indispensable Cellular Player in Bone Metastasis Process

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