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Cancers
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Effects of TGF-Beta on Cancer Cell Metabolism
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Effects of TGF-Beta on Cancer Cell Metabolism

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Cancer Immunology and Immunotherapy".

Deadline for manuscript submissions: closed (15 August 2022) | Viewed by 19278

Special Issue Editors

Dr. Loredana Bergandi

E-Mail Website
Guest Editor
Department of Oncology, University of Torino, via Santena 5 bis, 10126 Torino, Italy
Interests: nitric oxide; oxidative/nitrosative stress; in vitro bioglass compatibility; asbestos; epithelial–mesenchymal transition; oocytes competence; metabolic shift; chemoresistance
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Francesca Silvagno

E-Mail Website
Guest Editor
Department of Oncology, University of Torino, Via Santena 5 bis, 10126 Torino, Italy
Interests: cancer metabolism; vitamin D; TGF beta; mitochondrial metabolism; biochemistry; electromagnetic field; cancer growth; dermal wound healing; nutraceuticals
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Transforming growth factor (TGF)-β and the members of the relative superfamily play a central role in cancer. In fact, these cytokines are ubiquitously produced and act on many different cell types in a pleiotropic manner. Virtually every type of cancer is exposed to TGF-β, which by paracrine or autocrine mechanisms triggers a context-specific response. As a consequence, TGF-β has been defined as an inflammatory mediator, a tumor suppressor, a tumor promoter, an inducer of epithelial–epithelial–mesenchymal transition, a pro-fibrotic agent, and a metabolic reprogramming cytokine.

While the complex nuclear signaling of TGF-β has been widely investigated, the metabolic effects of the cytokine are the latest focus of the scientific community. Many valuable studies have revealed details on the control exerted by TGF-β on energy production, biosynthetic pathways, redox balance, and invasiveness of cancer cells, but the information is at the moment limited and scattered over various cancer models. A global picture of the general meaning of TGF-β is still missing. Further understanding of TGF-β activity is vital to develop new therapeutic strategies to improve cancer treatment and patient survival.

This Special Issue of Cancers therefore encompasses new research articles and timely reviews on all aspects of metabolic influence of TGF-β and related family members on cancer cells and their microenvironment, and on new possible approaches for cancer treatment, including metabolic modifiers, targeted and immune therapy, natural, pharmacological, and epigenetic modulators of TGF-β activity, and their impact on cancer metabolism.

Dr. Loredana Bergandi
Dr. Francesca Silvagno
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

 

Keywords

  • transforming growth factor (TGF)-β family
  • cancer cell metabolism
  • cancer growth
  • biosynthetic pathways
  • catabolic pathways
  • mitochondrial activity
  • immune system
  • inflammation
  • fibrosis
  • metabolites
  • redox homeostasis
  • tumor microenvironment
  • epigenetic modulation
  • epithelial–mesenchymal transition

Published Papers (5 papers)

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Research

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17 pages, 2766 KiB  
Article
TGF Beta Induces Vitamin D Receptor and Modulates Mitochondrial Activity of Human Pancreatic Cancer Cells
by Camilla Fiz, Giulia Apprato, Chiara Ricca, Alessia Aillon, Loredana Bergandi and Francesca Silvagno
Cancers 2021, 13(12), 2932; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers13122932 - 11 Jun 2021
Cited by 5 | Viewed by 2569
Abstract
The inflammatory cytokine TGFβ is both a tumor suppressor during cancer initiation and a promoter of metastasis along cancer progression. Inflammation and cancer are strictly linked, and cancer onset often correlates with the insufficiency of vitamin D, known for its anti-inflammatory properties. In [...] Read more.
The inflammatory cytokine TGFβ is both a tumor suppressor during cancer initiation and a promoter of metastasis along cancer progression. Inflammation and cancer are strictly linked, and cancer onset often correlates with the insufficiency of vitamin D, known for its anti-inflammatory properties. In this study, we investigated the interplay between TGFβ and vitamin D in two models of human pancreatic cancer, and we analyzed the metabolic effects of a prolonged TGFβ treatment mimicking the inflammatory environment of pancreatic cancer in vivo. We confirmed the induction of the vitamin D receptor previously described in epithelial cells, but the inhibitory effects of vitamin D on epithelial–mesenchymal transition (EMT) were lost when the hormone was given after a long treatment with TGFβ. Moreover, we detected an ROS-mediated toxicity of the acute treatment with TGFβ, whereas a chronic exposure to low doses had a protumorigenic effect. In fact, it boosted the mitochondrial respiration and cancer cell migration without ROS production and cytotoxicity. Our observations shed some light on the multifaceted role of TGFβ in tumor progression, revealing that a sustained exposure to TGFβ at low doses results in an irreversibly increased EMT associated with a metabolic modulation which favors the formation of metastasis. Full article
(This article belongs to the Special Issue Effects of TGF-Beta on Cancer Cell Metabolism)
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Review

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15 pages, 660 KiB  
Review
NUAK1 and NUAK2 Fine-Tune TGF-β Signaling
by Reinofke A. J. van de Vis, Aristidis Moustakas and Lars P. van der Heide
Cancers 2021, 13(13), 3377; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers13133377 - 05 Jul 2021
Cited by 11 | Viewed by 5224
Abstract
Transforming growth factor-β (TGF-β) signaling plays a key role in governing various cellular processes, extending from cell proliferation and apoptosis to differentiation and migration. Due to this extensive involvement in the regulation of cellular function, aberrant TGF-β signaling is frequently implicated in the [...] Read more.
Transforming growth factor-β (TGF-β) signaling plays a key role in governing various cellular processes, extending from cell proliferation and apoptosis to differentiation and migration. Due to this extensive involvement in the regulation of cellular function, aberrant TGF-β signaling is frequently implicated in the formation and progression of tumors. Therefore, a full understanding of the mechanisms of TGF-β signaling and its key components will provide valuable insights into how this intricate signaling cascade can shift towards a detrimental course. In this review, we discuss the interplay between TGF-β signaling and the AMP-activated protein kinase (AMPK)-related NUAK kinase family. We highlight the function and regulation of these kinases with focus on the pivotal role NUAK1 and NUAK2 play in regulating TGF-β signaling. Specifically, TGF-β induces the expression of NUAK1 and NUAK2 that regulates TGF-β signaling output in an opposite manner. Besides the focus on the TGF-β pathway, we also present a broader perspective on the expression and signaling interactions of the NUAK kinases to outline the broader functions of these protein kinases. Full article
(This article belongs to the Special Issue Effects of TGF-Beta on Cancer Cell Metabolism)
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13 pages, 1016 KiB  
Review
Transforming Growth Factor-β and Oxidative Stress in Cancer: A Crosstalk in Driving Tumor Transformation
by Valeria Ramundo, Giuliana Giribaldi and Elisabetta Aldieri
Cancers 2021, 13(12), 3093; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers13123093 - 21 Jun 2021
Cited by 21 | Viewed by 3214
Abstract
Cancer metabolism involves different changes at a cellular level, and altered metabolic pathways have been demonstrated to be heavily involved in tumorigenesis and invasiveness. A crucial role for oxidative stress in cancer initiation and progression has been demonstrated; redox imbalance, due to aberrant [...] Read more.
Cancer metabolism involves different changes at a cellular level, and altered metabolic pathways have been demonstrated to be heavily involved in tumorigenesis and invasiveness. A crucial role for oxidative stress in cancer initiation and progression has been demonstrated; redox imbalance, due to aberrant reactive oxygen species (ROS) production or deregulated efficacy of antioxidant systems (superoxide dismutase, catalase, GSH), contributes to tumor initiation and progression of several types of cancer. ROS may modulate cancer cell metabolism by acting as secondary messengers in the signaling pathways (NF-kB, HIF-1α) involved in cellular proliferation and metastasis. It is known that ROS mediate many of the effects of transforming growth factor β (TGF-β), a key cytokine central in tumorigenesis and cancer progression, which in turn can modulate ROS production and the related antioxidant system activity. Thus, ROS synergize with TGF-β in cancer cell metabolism by increasing the redox imbalance in cancer cells and by inducing the epithelial mesenchymal transition (EMT), a crucial event associated with tumor invasiveness and metastases. Taken as a whole, this review is addressed to better understanding this crosstalk between TGF-β and oxidative stress in cancer cell metabolism, in the attempt to improve the pharmacological and therapeutic approach against cancer. Full article
(This article belongs to the Special Issue Effects of TGF-Beta on Cancer Cell Metabolism)
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21 pages, 1288 KiB  
Review
TGF-β in Cancer: Metabolic Driver of the Tolerogenic Crosstalk in the Tumor Microenvironment
by Roberta Angioni, Ricardo Sánchez-Rodríguez, Antonella Viola and Barbara Molon
Cancers 2021, 13(3), 401; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers13030401 - 22 Jan 2021
Cited by 35 | Viewed by 4273
Abstract
Overcoming tumor immunosuppression still represents one ambitious achievement for cancer immunotherapy. Of note, the cytokine TGF-β contributes to immune evasion in multiple cancer types, by feeding the establishment of a tolerogenic environment in the host. Indeed, it fosters the expansion and accumulation of [...] Read more.
Overcoming tumor immunosuppression still represents one ambitious achievement for cancer immunotherapy. Of note, the cytokine TGF-β contributes to immune evasion in multiple cancer types, by feeding the establishment of a tolerogenic environment in the host. Indeed, it fosters the expansion and accumulation of immunosuppressive regulatory cell populations within the tumor microenvironment (TME), where it also activates resident stromal cells and enhances angiogenesis programs. More recently, TGF-β has also turned out as a key metabolic adjuster in tumors orchestrating metabolic pathways in the TME. In this review, we will scrutinize TGF-β-mediated immune and stromal cell crosstalk within the TME, with a primary focus on metabolic programs. Full article
(This article belongs to the Special Issue Effects of TGF-Beta on Cancer Cell Metabolism)
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24 pages, 3565 KiB  
Review
Therapeutic Implications of TGFβ in Cancer Treatment: A Systematic Review
by Verónica Gómez-Gil
Cancers 2021, 13(3), 379; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers13030379 - 20 Jan 2021
Cited by 13 | Viewed by 2739
Abstract
Transforming growth factor β (TGFβ) is a pleiotropic cytokine that participates in a wide range of biological functions. The alterations in the expression levels of this factor, or the deregulation of its signaling cascade, can lead to different pathologies, including cancer. A great [...] Read more.
Transforming growth factor β (TGFβ) is a pleiotropic cytokine that participates in a wide range of biological functions. The alterations in the expression levels of this factor, or the deregulation of its signaling cascade, can lead to different pathologies, including cancer. A great variety of therapeutic strategies targeting TGFβ, or the members included in its signaling pathway, are currently being researched in cancer treatment. However, the dual role of TGFβ, as a tumor suppressor or a tumor-promoter, together with its crosstalk with other signaling pathways, has hampered the development of safe and effective treatments aimed at halting the cancer progression. This systematic literature review aims to provide insight into the different approaches available to regulate TGFβ and/or the molecules involved in its synthesis, activation, or signaling, as a cancer treatment. The therapeutic strategies most commonly investigated include antisense oligonucleotides, which prevent TGFβ synthesis, to molecules that block the interaction between TGFβ and its signaling receptors, together with inhibitors of the TGFβ signaling cascade-effectors. The effectiveness and possible complications of the different potential therapies available are also discussed. Full article
(This article belongs to the Special Issue Effects of TGF-Beta on Cancer Cell Metabolism)
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