Special Issue "Cell Cycle Deregulation in Cancers"

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

Deadline for manuscript submissions: closed (15 October 2013)

Special Issue Editor

Guest Editor
Dr. Rebecca S. Hartley (Website)

Department of Cell Biology and Physiology; MSC08-4750; University of New Mexico; Albuquerque, NM 87131, USA
Phone: 505-272-4009
Interests: cell cycle; cyclins; cyclin/CDKs; post-transcriptional control of gene expression; RNA binding proteins; microRNAs; cell cycle deregulation in cancer; developmental basis of cancer; microenvironmental control of the cell cycle

Special Issue Information

Dear Colleagues,

Loss of normal cell cycle control is a hallmark of cancer, resulting in targeting of cell cycle regulators for cancer therapy. In general, strategies used to exploit the deregulated cancer cell cycle by directly targeting cell cycle regulators do not provide cancer specificity. This issue of Cancers invites contributions of original research reports, clinical studies, and review articles that focus on cancer specific modifications that would allow indirect targeting of cell cycle deregulation. Potential topics include modifications of the microenvironment, inflammatory signaling, stress response, and post-transcriptional events that result in cell cycle deregulation.

Dr. Rebecca S. Hartley
Guest Editor

Submission

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. Papers will be published continuously (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 refereed through a 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 monthly 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 800 CHF (Swiss Francs).

Keywords

  • cell cycle regulators
  • cell cycle deregulation
  • cancer cell cycle
  • cancer specific modifications
  • cancer vulnerabilities
  • cancer therapy
  • tumor microenvironment
  • inflammatory signaling
  • stress response
  • post-transcription

Published Papers (5 papers)

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Research

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Open AccessArticle The Role of the 3' Untranslated Region in the Post-Transcriptional Regulation of KLF6 Gene Expression in Hepatocellular Carcinoma
Cancers 2014, 6(1), 28-41; doi:10.3390/cancers6010028
Received: 17 October 2013 / Revised: 25 November 2013 / Accepted: 26 November 2013 / Published: 19 December 2013
Cited by 1 | PDF Full-text (602 KB) | HTML Full-text | XML Full-text
Abstract
KLF6 is ubiquitously expressed in human tissues and regulates many pathways such as differentiation, development, cellular proliferation, growth-related signal transduction, and apoptosis. We previously demonstrated that KLF6 expression is altered during liver carcinogenesis. More importantly, KLF6 invalidation results in cell cycle progression [...] Read more.
KLF6 is ubiquitously expressed in human tissues and regulates many pathways such as differentiation, development, cellular proliferation, growth-related signal transduction, and apoptosis. We previously demonstrated that KLF6 expression is altered during liver carcinogenesis. More importantly, KLF6 invalidation results in cell cycle progression inhibition and apoptosis of liver cancer cells. On the other hand, enforced expression of KLF6 variant 2 (SV2) induces cancer cell death by apoptosis. Thus, we and others demonstrated that KLF6 and its splicing variants play a critical role in liver cancer. However, little is known on the mechanisms governing KLF6 expression in HCC. In the present work, we asked whether the 3' untranslated region (3'UTR) of the KLF6 mRNA may be responsible for regulation of KLF6 expression in HCC. We found that KLF6 mRNA stability was altered in liver-derived cell lines as compared to cervical cancer-derived cell lines and human embryonic fibroblasts. Interestingly, KLF6 mRNA was highly unstable in liver cancer-derived cell lines as compared to normal hepatocytes. We next cloned the KLF6 mRNA 3'UTR into luciferase-expressing vectors and found that gene expression and activity were strongly impaired in all liver-derived cell lines tested. In addition, we found that most the KLF6 3'UTR destabilisation activity resides between nt 1,835 and nt 2,615 of the KLF6 gene. Taken together, we provide the first steps towards better understanding of the regulation of KLF6 expression in HCC. Further work is needed to identify the factors that bind to KLF6 3'UTR to regulate its expression in liver cancer-derived cell lines. Full article
(This article belongs to the Special Issue Cell Cycle Deregulation in Cancers)

Review

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Open AccessReview p53 Acetylation: Regulation and Consequences
Cancers 2015, 7(1), 30-69; doi:10.3390/cancers7010030
Received: 18 March 2014 / Accepted: 12 December 2014 / Published: 23 December 2014
Cited by 10 | PDF Full-text (1218 KB) | HTML Full-text | XML Full-text
Abstract
Post-translational modifications of p53 are critical in modulating its tumor suppressive functions. Ubiquitylation, for example, plays a major role in dictating p53 stability, subcellular localization and transcriptional vs. non-transcriptional activities. Less is known about p53 acetylation. It has been shown to govern [...] Read more.
Post-translational modifications of p53 are critical in modulating its tumor suppressive functions. Ubiquitylation, for example, plays a major role in dictating p53 stability, subcellular localization and transcriptional vs. non-transcriptional activities. Less is known about p53 acetylation. It has been shown to govern p53 transcriptional activity, selection of growth inhibitory vs. apoptotic gene targets, and biological outcomes in response to diverse cellular insults. Yet recent in vivo evidence from mouse models questions the importance of p53 acetylation (at least at certain sites) as well as canonical p53 functions (cell cycle arrest, senescence and apoptosis) to tumor suppression. This review discusses the cumulative findings regarding p53 acetylation, with a focus on the acetyltransferases that modify p53 and the mechanisms regulating their activity. We also evaluate what is known regarding the influence of other post-translational modifications of p53 on its acetylation, and conclude with the current outlook on how p53 acetylation affects tumor suppression. Due to redundancies in p53 control and growing understanding that individual modifications largely fine-tune p53 activity rather than switch it on or off, many questions still remain about the physiological importance of p53 acetylation to its role in preventing cancer. Full article
(This article belongs to the Special Issue Cell Cycle Deregulation in Cancers)
Open AccessReview Situational Awareness: Regulation of the Myb Transcription Factor in Differentiation, the Cell Cycle and Oncogenesis
Cancers 2014, 6(4), 2049-2071; doi:10.3390/cancers6042049
Received: 4 May 2014 / Revised: 11 August 2014 / Accepted: 26 September 2014 / Published: 2 October 2014
Cited by 8 | PDF Full-text (984 KB) | HTML Full-text | XML Full-text
Abstract
This review summarizes the mechanisms that control the activity of the c-Myb transcription factor in normal cells and tumors, and discusses how c-Myb plays a role in the regulation of the cell cycle. Oncogenic versions of c-Myb contribute to the development of [...] Read more.
This review summarizes the mechanisms that control the activity of the c-Myb transcription factor in normal cells and tumors, and discusses how c-Myb plays a role in the regulation of the cell cycle. Oncogenic versions of c-Myb contribute to the development of leukemias and solid tumors such as adenoid cystic carcinoma, breast cancer and colon cancer. The activity and specificity of the c-Myb protein seems to be controlled through changes in protein-protein interactions, so understanding how it is regulated could lead to the development of novel therapeutic strategies. Full article
(This article belongs to the Special Issue Cell Cycle Deregulation in Cancers)
Open AccessReview The Complex Relationship between Liver Cancer and the Cell Cycle: A Story of Multiple Regulations
Cancers 2014, 6(1), 79-111; doi:10.3390/cancers6010079
Received: 14 November 2013 / Revised: 24 December 2013 / Accepted: 3 January 2014 / Published: 13 January 2014
Cited by 4 | PDF Full-text (1655 KB) | HTML Full-text | XML Full-text
Abstract
The liver acts as a hub for metabolic reactions to keep a homeostatic balance during development and growth. The process of liver cancer development, although poorly understood, is related to different etiologic factors like toxins, alcohol, or viral infection. At the molecular [...] Read more.
The liver acts as a hub for metabolic reactions to keep a homeostatic balance during development and growth. The process of liver cancer development, although poorly understood, is related to different etiologic factors like toxins, alcohol, or viral infection. At the molecular level, liver cancer is characterized by a disruption of cell cycle regulation through many molecular mechanisms. In this review, we focus on the mechanisms underlying the lack of regulation of the cell cycle during liver cancer, focusing mainly on hepatocellular carcinoma (HCC). We also provide a brief summary of novel therapies connected to cell cycle regulation. Full article
(This article belongs to the Special Issue Cell Cycle Deregulation in Cancers)
Open AccessReview Long Non-Coding RNAs Embedded in the Rb and p53 Pathways
Cancers 2013, 5(4), 1655-1675; doi:10.3390/cancers5041655
Received: 16 October 2013 / Revised: 12 November 2013 / Accepted: 20 November 2013 / Published: 4 December 2013
Cited by 5 | PDF Full-text (631 KB) | HTML Full-text | XML Full-text
Abstract
In recent years, long non-coding RNAs (lncRNAs) have gained significant attention as a novel class of gene regulators. Although a small number of lncRNAs have been shown to regulate gene expression through diverse mechanisms including transcriptional regulation, mRNA splicing and translation, the [...] Read more.
In recent years, long non-coding RNAs (lncRNAs) have gained significant attention as a novel class of gene regulators. Although a small number of lncRNAs have been shown to regulate gene expression through diverse mechanisms including transcriptional regulation, mRNA splicing and translation, the physiological function and mechanism of action of the vast majority are not known. Profiling studies in cell lines and tumor samples have suggested a potential role of lncRNAs in cancer. Indeed, distinct lncRNAs have been shown to be embedded in the p53 and Rb networks, two of the major tumor suppressor pathways that control cell cycle progression and survival. Given the fact that inactivation of Rb and p53 is a hallmark of human cancer, in this review we discuss recent evidence on the function of lncRNAs in the Rb and p53 signaling pathways. Full article
(This article belongs to the Special Issue Cell Cycle Deregulation in Cancers)

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