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Cancers
Special Issues
Senescence and Cancer
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Senescence and Cancer

A special issue of Cancers (ISSN 2072-6694).

Deadline for manuscript submissions: closed (31 May 2020) | Viewed by 47535

Special Issue Editors

Prof. Dr. Barbara L. Van Leeuwen

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Guest Editor
Department of Surgery, University Medical Center Groningen, Groningen University, Hanzeplein 1, 9700 RB Groningen, The Netherlands
Interests: Elderly; Surgery; Inflammation; Cognition; Music
Dr. Baukje Brattinga

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Guest Editor
Department of Surgery, University Medical Center Groningen, Groningen University, Hanzeplein 1, 9700 RB Groningen, The Netherlands
Interests: elderly; inflammation; cellular senescence; surgery; senescence

Special Issue Information

Dear Colleagues,

Cellular senescence is one of the key elements of aging. Cellular senescence is an irreversible growth arrest in cell proliferation, which is induced by potential oncogenic stimuli, such as DNA damage or oncogene activation. Senescent cells are characterized by changes in gene expression, in particular the activation of the senescence-associated secretory phenotype (SASP), which can result in different effects. The acute senescence response induces an inflammatory response, promotes tissue repair, and suppresses tumor genesis. Chronic cellular senescence is a degenerative response and a switch from temporal to persistent cell-cycle arrest. Chronic cellular senescence is increased in aging and age-related diseases, such as cancer.

In this Special Issue on senescence and cancer, we focus on the current knowledge on the relationship between senescence and cancer, the possible prognostic value of senescent cells, and possible targets for intervention.

Prof. Dr. Barbara L. Van Leeuwen
Dr. Baukje Brattinga
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 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

  • Cellular senescence
  • elements of aging
  • oncogenic stimuli
  • DNA damage
  • oncogene activation
  • senescence-associated secretory phenotype (SASP)
  • acute senescence
  • Chronic cellular senescence
  • cancer

Published Papers (7 papers)

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Editorial

Jump to: Research, Review

2 pages, 166 KiB  
Editorial
Senescent Cells: A Potential Target for New Cancer Therapies in Older Oncologic Patients
by Baukje Brattinga and Barbara L. van Leeuwen
Cancers 2021, 13(2), 278; https://doi.org/10.3390/cancers13020278 - 13 Jan 2021
Cited by 3 | Viewed by 1595
Abstract
Cellular senescence is a complex process and is one of the key elements of ageing [...] Full article
(This article belongs to the Special Issue Senescence and Cancer)

Research

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18 pages, 4787 KiB  
Article
Cancer Stem Cell-Inducing Media Activates Senescence Reprogramming in Fibroblasts
by Patrick M. Perrigue, Magdalena Rakoczy, Kamila P. Pawlicka, Agnieszka Belter, Małgorzata Giel-Pietraszuk, Mirosława Naskręt-Barciszewska, Jan Barciszewski and Marek Figlerowicz
Cancers 2020, 12(7), 1745; https://doi.org/10.3390/cancers12071745 - 30 Jun 2020
Cited by 15 | Viewed by 5470
Abstract
Cellular senescence is a tumor-suppressive mechanism blocking cell proliferation in response to stress. However, recent evidence suggests that senescent tumor cells can re-enter the cell cycle to become cancer stem cells, leading to relapse after cancer chemotherapy treatment. Understanding how the senescence reprogramming [...] Read more.
Cellular senescence is a tumor-suppressive mechanism blocking cell proliferation in response to stress. However, recent evidence suggests that senescent tumor cells can re-enter the cell cycle to become cancer stem cells, leading to relapse after cancer chemotherapy treatment. Understanding how the senescence reprogramming process is a precursor to cancer stem cell formation is of great medical importance. To study the interplay between senescence, stemness, and cancer, we applied a stem cell medium (SCM) to human embryonic fibroblasts (MRC5 and WI-38) and cancer cell lines (A549 and 293T). MRC5 and WI-38 cells treated with SCM showed symptoms of oxidative stress and became senescent. Transcriptome analysis over a time course of SCM-induced senescence, revealed a developmental process overlapping with the upregulation of genes for growth arrest and the senescence-associated secretory phenotype (SASP). We demonstrate that histone demethylases jumonji domain-containing protein D3 (Jmjd3) and ubiquitously transcribed tetratricopeptide repeat, X chromosome (Utx), which operate by remodeling chromatin structure, are implicated in the senescence reprogramming process to block stem cell formation in fibroblasts. In contrast, A549 and 293T cells cultured in SCM were converted to cancer stem cells that displayed the phenotype of senescence uncoupled from growth arrest. The direct overexpression of DNA methyltransferases (Dnmt1 and Dnmt3A), ten-eleven translocation methylcytosine dioxygenases (Tet1 and Tet3), Jmjd3, and Utx proteins could activate senescence-associated beta-galactosidase (SA-β-gal) activity in 293T cells, suggesting that epigenetic alteration and chromatin remodeling factors trigger the senescence response. Overall, our study suggests that chromatin machinery controlling senescence reprogramming is significant in cancer stem cell formation. Full article
(This article belongs to the Special Issue Senescence and Cancer)
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22 pages, 4042 KiB  
Article
HuRdling Senescence: HuR Breaks BRAF-Induced Senescence in Melanocytes and Supports Melanoma Growth
by Janika K. Liebig, Silke Kuphal and Anja Katrin Bosserhoff
Cancers 2020, 12(5), 1299; https://doi.org/10.3390/cancers12051299 - 21 May 2020
Cited by 15 | Viewed by 3828
Abstract
In addition to genetic changes, post-transcriptional events strongly contribute to the progression of malignant tumors. The RNA-binding protein HuR (ELAVL1) is able to bind and stabilize a large group of target mRNAs, which contain AU-rich elements (ARE) in their 3′-untranslated region. [...] Read more.
In addition to genetic changes, post-transcriptional events strongly contribute to the progression of malignant tumors. The RNA-binding protein HuR (ELAVL1) is able to bind and stabilize a large group of target mRNAs, which contain AU-rich elements (ARE) in their 3′-untranslated region. We found HuR to be upregulated in malignant melanoma in vitro and in vivo, significantly correlating with progression in vivo. Additionally, we could show that miR-194-5p can regulate HuR expression level. HuR knockdown in melanoma cells led to the suppression of proliferation and the induction of cellular senescence. Interestingly, HuR overexpression was sufficient to inhibit senescence in BRAFV600E-expressing melanocytes and to force their growth. Here, MITF (Microphthalmia-associated transcription factor), a key player in suppressing senescence and an ARE containing transcript, is positively regulated by HuR. Our results show for the first time that the overexpression of HuR is an important part of the regulatory pathway in the development of malignant melanoma and functions as a switch to overcome oncogene-induced senescence and to support melanoma formation. These newly defined alterations may provide possibilities for innovative therapeutic approaches. Full article
(This article belongs to the Special Issue Senescence and Cancer)
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Review

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20 pages, 853 KiB  
Review
Senescence and Cancer: A Review of Clinical Implications of Senescence and Senotherapies
by Lynda Wyld, Ilaria Bellantuono, Tamara Tchkonia, Jenna Morgan, Olivia Turner, Fiona Foss, Jayan George, Sarah Danson and James L. Kirkland
Cancers 2020, 12(8), 2134; https://doi.org/10.3390/cancers12082134 - 31 Jul 2020
Cited by 142 | Viewed by 11979
Abstract
Cellular senescence is a key component of human aging that can be induced by a range of stimuli, including DNA damage, cellular stress, telomere shortening, and the activation of oncogenes. Senescence is generally regarded as a tumour suppressive process, both by preventing cancer [...] Read more.
Cellular senescence is a key component of human aging that can be induced by a range of stimuli, including DNA damage, cellular stress, telomere shortening, and the activation of oncogenes. Senescence is generally regarded as a tumour suppressive process, both by preventing cancer cell proliferation and suppressing malignant progression from pre-malignant to malignant disease. It may also be a key effector mechanism of many types of anticancer therapies, such as chemotherapy, radiotherapy, and endocrine therapies, both directly and via bioactive molecules released by senescent cells that may stimulate an immune response. However, senescence may contribute to reduced patient resilience to cancer therapies and may provide a pathway for disease recurrence after cancer therapy. A new group of drugs, senotherapies, (drugs which interact with senescent cells to interfere with their pro-aging impacts by either selectively destroying senescent cells (senolytic drugs) or inhibiting their function (senostatic drugs)) are under active investigation to determine whether they can enhance the efficacy of cancer therapies and improve resilience to cancer treatments. Senolytic drugs include quercetin, navitoclax, and fisetin and preclinical and early phase clinical data are emerging of their potential role in cancer treatments, although none are yet in routine use clinically. This article provides a review of these issues. Full article
(This article belongs to the Special Issue Senescence and Cancer)
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22 pages, 671 KiB  
Review
The Premature Senescence in Breast Cancer Treatment Strategy
by Małgorzata Milczarek
Cancers 2020, 12(7), 1815; https://doi.org/10.3390/cancers12071815 - 6 Jul 2020
Cited by 26 | Viewed by 5188
Abstract
Cellular senescence is a permanent blockade of cell proliferation. In response to therapy-induced stress, cancer cells undergo apoptosis or premature senescence. In apoptosis-resistant cancer cells or at lower doses of anticancer drugs, therapy-induced stress leads to premature senescence. The role of this senescence [...] Read more.
Cellular senescence is a permanent blockade of cell proliferation. In response to therapy-induced stress, cancer cells undergo apoptosis or premature senescence. In apoptosis-resistant cancer cells or at lower doses of anticancer drugs, therapy-induced stress leads to premature senescence. The role of this senescence in cancer treatment is discussable. First of all, the senescent cells lose the ability to proliferate, migrate, and invade. In addition, the senescent cells secrete a set of proteins (inflammatory cytokines, chemokines, growth factors) known as the senescence-associated secretory phenotype (SASP), which influences non-senescent normal cells and non-senescent cancer cells in the tumor microenvironment and triggers tumor promotion and recurrence. Recently, many studies have examined senescence induction through breast cancer therapy and potentially using this phenomenon to treat this cancer. This review summarizes the recent in vitro, in vivo, and clinical studies investigating senescence in breast cancer treatments. Senescence inductors, senolytics, as well as their action mechanism are discussed herein. Potential SASP-modulating treatment strategies are also described. Full article
(This article belongs to the Special Issue Senescence and Cancer)
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19 pages, 695 KiB  
Review
Senescence and Cancer: Role of Nitric Oxide (NO) in SASP
by Nesrine Mabrouk, Silvia Ghione, Véronique Laurens, Stéphanie Plenchette, Ali Bettaieb and Catherine Paul
Cancers 2020, 12(5), 1145; https://doi.org/10.3390/cancers12051145 - 2 May 2020
Cited by 14 | Viewed by 4268
Abstract
Cellular senescence is a cell state involved in both physiological and pathological processes such as age-related diseases and cancer. While the mechanism of senescence is now well known, its role in tumorigenesis still remains very controversial. The positive and negative effects of senescence [...] Read more.
Cellular senescence is a cell state involved in both physiological and pathological processes such as age-related diseases and cancer. While the mechanism of senescence is now well known, its role in tumorigenesis still remains very controversial. The positive and negative effects of senescence on tumorigenesis depend largely on the diversity of the senescent phenotypes and, more precisely, on the senescence-associated secretory phenotype (SASP). In this review, we discuss the modulatory effect of nitric oxide (NO) in SASP and the possible benefits of the use of NO donors or iNOS inducers in combination with senotherapy in cancer treatment. Full article
(This article belongs to the Special Issue Senescence and Cancer)
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38 pages, 550 KiB  
Review
Therapy-Induced Senescence: An “Old” Friend Becomes the Enemy
by Tareq Saleh, Sarah Bloukh, Valerie J. Carpenter, Enas Alwohoush, Jomana Bakeer, Sarah Darwish, Belal Azab and David A. Gewirtz
Cancers 2020, 12(4), 822; https://doi.org/10.3390/cancers12040822 - 29 Mar 2020
Cited by 172 | Viewed by 13983
Abstract
For the past two decades, cellular senescence has been recognized as a central component of the tumor cell response to chemotherapy and radiation. Traditionally, this form of senescence, termed Therapy-Induced Senescence (TIS), was linked to extensive nuclear damage precipitated by classical genotoxic chemotherapy. [...] Read more.
For the past two decades, cellular senescence has been recognized as a central component of the tumor cell response to chemotherapy and radiation. Traditionally, this form of senescence, termed Therapy-Induced Senescence (TIS), was linked to extensive nuclear damage precipitated by classical genotoxic chemotherapy. However, a number of other forms of therapy have also been shown to induce senescence in tumor cells independently of direct genomic damage. This review attempts to provide a comprehensive summary of both conventional and targeted anticancer therapeutics that have been shown to induce senescence in vitro and in vivo. Still, the utility of promoting senescence as a therapeutic endpoint remains under debate. Since senescence represents a durable form of growth arrest, it might be argued that senescence is a desirable outcome of cancer therapy. However, accumulating evidence suggesting that cells have the capacity to escape from TIS would support an alternative conclusion, that senescence provides an avenue whereby tumor cells can evade the potentially lethal action of anticancer drugs, allowing the cells to enter a temporary state of dormancy that eventually facilitates disease recurrence, often in a more aggressive state. Furthermore, TIS is now strongly connected to tumor cell remodeling, potentially to tumor dormancy, acquiring more ominous malignant phenotypes and accounts for several untoward adverse effects of cancer therapy. Here, we argue that senescence represents a barrier to effective anticancer treatment, and discuss the emerging efforts to identify and exploit agents with senolytic properties as a strategy for elimination of the persistent residual surviving tumor cell population, with the goal of mitigating the tumor-promoting influence of the senescent cells and to thereby reduce the likelihood of cancer relapse. Full article
(This article belongs to the Special Issue Senescence and Cancer)
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