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Cells
Special Issues
Interconnection between Senescence and Cancer
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Interconnection between Senescence and Cancer

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Aging".

Deadline for manuscript submissions: closed (31 December 2022) | Viewed by 10209

Special Issue Editors

Dr. Yasumichi Inoue

E-Mail Website
Guest Editor
Graduate School of Pharmaceutical Sciences, Nagoya City University, Nagoya, Japan
Interests: cancer; cell cycle; cellular senescence; endoplasmic reticulum stress; molecular target drugs; p53; transcriptional regulation
Special Issues, Collections and Topics in MDPI journals
Dr. Chi-Ming Wong

E-Mail Website
Guest Editor
Department of Pharmacology and Pharmacy, Hong Kong Polytechnic University, Kowloon, Hong Kong, China
Interests: antioxidants; peroxiredoxins; oxidative stress; growth factors and hormones; transcription and translation regulation
Dr. Andy T. Y. Lau

E-Mail Website
Guest Editor
Department of Cell Biology and Genetics, Shantou University Medical College, Shantou, China
Interests: cancer proteomics; epigenetic toxicology; epimodifications; epimutagenesis; epithelial-mesenchymal plasticity

Special Issue Information

Dear Colleagues,

Cellular senescence occurs in response to various stressors, including DNA damage, oxidative stress and oncogene activation. Senescence acts primarily as a tumour suppression mechanism that prevents proliferation of potentially cancerous cells. Senescence cells secrete plethora of factors, including inflammatory cytokines, growth factors, and proteases, collectively known as the senescence-asscociated secretory phenotype (SASP). SASP can stimulate immunosurveillance mechanisms and potent the tumor suppresive function of senescent cells. On the other hand, the accumulation of senescent cells in vivo exerts detrimental effects on the functionality of tissues and organs. Chronic accumulation of senescent cells also promote tumor relapse and metastasis. Thus, the Jekyll and Hyde nature of cellular senescence is highly complex, and understanding the regulatory mechanisms of cellular senescence will lead to the development of therapies for various diseases, including cancer, neurodegenerative diseases and diabetes. This Special Issue provides an open access forum aimed at compiling a collection of original research and review articles on the interconnection between senescence and cancer.

Dr. Yasumichi Inoue
Dr. Chi-Ming Wong
Dr. Andy T. Y. Lau
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. Cells 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 2700 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

  • apoptosis
  • cancer
  • cell cycle
  • DNA damage
  • metabolic diseases
  • oxidative stress
  • senolysis
  • senescence
  • therapeutic approach

Published Papers (3 papers)

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Research

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17 pages, 4585 KiB  
Article
Notch3 Transactivates Glycogen Synthase Kinase-3-Beta and Inhibits Epithelial-to-Mesenchymal Transition in Breast Cancer Cells
by Weiling Chen, Yongqu Zhang, Ronghui Li, Wenhe Huang, Xiaolong Wei, De Zeng, Yuanke Liang, Yunzhu Zeng, Min Chen, Lixin Zhang, Wenliang Gao, Yuanyuan Zhu, Yaochen Li and Guojun Zhang
Cells 2022, 11(18), 2872; https://doi.org/10.3390/cells11182872 - 14 Sep 2022
Cited by 3 | Viewed by 1803
Abstract
As a critical transformational process in the attributes of epithelial cells, epithelial-to-mesenchymal transition (EMT) is involved in tumor invasion, metastasis, and resistance to treatment, which contributes to the ultimate death of some patients with breast cancer. Glycogen synthase kinase-3-beta (GSK3β) is thought to [...] Read more.
As a critical transformational process in the attributes of epithelial cells, epithelial-to-mesenchymal transition (EMT) is involved in tumor invasion, metastasis, and resistance to treatment, which contributes to the ultimate death of some patients with breast cancer. Glycogen synthase kinase-3-beta (GSK3β) is thought to be an EMT suppressor that down-regulates the protein, snail, a zinc finger transcription inhibitor, and regulates E-cadherin expression and the Wnt signaling pathway. Our previous studies have shown that Notch3 also inhibits EMT in breast cancer. In mammary gland cells, GSK3β physically bound and phosphorylated the intracellular domain of two Notch paralogs: N1ICD was positively regulated, but N2ICD was negatively regulated; however, the relationship between Notch3, GSK3β, and EMT in breast cancer is still unclear and crosstalk between Notch3 and GSK3β has not been widely investigated. In this study, we revealed that Notch3 was an essential antagonist of EMT in breast cancer cells by transcriptionally upregulating GSK3β. In breast cancer, MCF-7 and MDA-MB-231 cell lines, the silencing of Notch3 reduced GSK3β expression, which is sufficient to induce EMT. Conversely, ectopic Notch3 expression re-activated GSK3β and E-cadherin. Mechanistically, Notch3 can bind to the GSK3β promoter directly and activate GSK3β transcription. In human breast cancer samples, Notch3 expression is positively associated with GSK3β (r = 0.416, p = 0.001); moreover, high expressions of Notch3 and GSK3β mRNA are correlated to better relapse-free survival in all breast cancer patients via analysis in “the Kaplan–Meier plotter” database. In summary, our preliminary results suggested that Notch3 might inhibit EMT by trans-activating GSK3β in breast cancer cells. The suppression of Notch3 expression may contribute to EMT by transcriptionally downregulating GSK3β in breast cancer. Full article
(This article belongs to the Special Issue Interconnection between Senescence and Cancer)
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21 pages, 9181 KiB  
Article
Artesunate Inhibits the Cell Growth in Colorectal Cancer by Promoting ROS-Dependent Cell Senescence and Autophagy
by Zhiying Huang, Shu Gan, Xuerong Zhuang, Yao Chen, Linlin Lu, Ying Wang, Xiaoxiao Qi, Qian Feng, Qiuju Huang, Biaoyan Du, Rong Zhang and Zhongqiu Liu
Cells 2022, 11(16), 2472; https://doi.org/10.3390/cells11162472 - 09 Aug 2022
Cited by 18 | Viewed by 3519
Abstract
Although artesunate has been reported to be a promising candidate for colorectal cancer (CRC) treatment, the underlying mechanisms and molecular targets of artesunate are yet to be explored. Here, we report that artesunate acts as a senescence and autophagy inducer to exert its [...] Read more.
Although artesunate has been reported to be a promising candidate for colorectal cancer (CRC) treatment, the underlying mechanisms and molecular targets of artesunate are yet to be explored. Here, we report that artesunate acts as a senescence and autophagy inducer to exert its inhibitory effect on CRC in a reactive oxygen species (ROS)-dependent manner. In SW480 and HCT116 cells, artesunate treatment led to mitochondrial dysfunction, drastically promoted mitochondrial ROS generation, and consequently inhibited cell proliferation by causing cell cycle arrest at G0/G1 phase as well as subsequent p16- and p21-mediated cell senescence. Senescent cells underwent endoplasmic reticulum stress (ERS), and the unfolded protein response (UPR) was activated via IRE1α signaling, with upregulated BIP, IRE1α, phosphorylated IRE1α (p-IRE1α), CHOP, and DR5. Further experiments revealed that autophagy was induced by artesunate treatment due to oxidative stress and ER stress. In contrast, N-Acetylcysteine (NAC, an ROS scavenger) and 3-Methyladenine (3-MA, an autophagy inhibitor) restored cell viability and attenuated autophagy in artesunate-treated cells. Furthermore, cellular free Ca2+ levels were increased and could be repressed by NAC, 3-MA, and GSK2350168 (an IRE1α inhibitor). In vivo, artesunate administration reduced the growth of CT26 cell-derived tumors in BALB/c mice. Ki67 and cyclin D1 expression was downregulated in tumor tissue, while p16, p21, p-IRE1α, and LC3B expression was upregulated. Taken together, artesunate induces senescence and autophagy to inhibit cell proliferation in colorectal cancer by promoting excessive ROS generation. Full article
(This article belongs to the Special Issue Interconnection between Senescence and Cancer)
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Review

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13 pages, 655 KiB  
Review
Peroxiredoxin, Senescence, and Cancer
by Mengyao Wu, Chujun Deng, Tak-Ho Lo, Ka-Ying Chan, Xiang Li and Chi-Ming Wong
Cells 2022, 11(11), 1772; https://doi.org/10.3390/cells11111772 - 28 May 2022
Cited by 15 | Viewed by 4188
Abstract
Peroxiredoxins are multifunctional enzymes that play a key role in protecting cells from stresses and maintaining the homeostasis of many cellular processes. Peroxiredoxins were firstly identified as antioxidant enzymes that can be found in all living organisms. Later studies demonstrated that peroxiredoxins also [...] Read more.
Peroxiredoxins are multifunctional enzymes that play a key role in protecting cells from stresses and maintaining the homeostasis of many cellular processes. Peroxiredoxins were firstly identified as antioxidant enzymes that can be found in all living organisms. Later studies demonstrated that peroxiredoxins also act as redox signaling regulators, chaperones, and proinflammatory factors and play important roles in oxidative defense, redox signaling, protein folding, cycle cell progression, DNA integrity, inflammation, and carcinogenesis. The versatility of peroxiredoxins is mainly based on their unique active center cysteine with a wide range of redox states and the ability to switch between low- and high-molecular-weight species for regulating their peroxidase and chaperone activities. Understanding the molecular mechanisms of peroxiredoxin in these processes will allow the development of new approaches to enhance longevity and to treat various cancers. In this article, we briefly review the history of peroxiredoxins, summarize recent advances in our understanding of peroxiredoxins in aging- and cancer-related biological processes, and discuss the future perspectives of using peroxiredoxins in disease diagnostics and treatments. Full article
(This article belongs to the Special Issue Interconnection between Senescence and Cancer)
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