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Akt and Its Role in DNA Damage Response (DDR) Pathways
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Akt and Its Role in DNA Damage Response (DDR) Pathways

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (31 December 2020)

Special Issue Editors

Prof. Dr. H. Peter Rodemann

E-Mail Website
Guest Editor
Division of Radiation Biology & Molecular Environmental Research, Department of Radiation Oncology, Eberhard Karls University Tuebingen, 72076 Tübingen, Germany
Interests: AKT; phosphorylation; radiation; DSB repair
Prof. Dr. Ekkehard Dikomey

E-Mail Website
Guest Editor
Laboratory of Radiobiology and Experimental Radiooncology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany

Special Issue Information

Dear Colleagues,

Akt signaling and DNA damage response pathways are major regulatory components of various mechanisms controlling cellular survival and genomic integrity. Moreover, genetic alterations resulting in aberrant activation of Akt have been recognized as a driving force of malignant transformation and cancer progression. Likewise, in recent years, accumulating evidence has indicated that Akt is directly involved in the regulation of DNA damage response pathways and specified DNA damage repair mechanisms responsible for DNA double strand as well as DNA single strand damage. Thus, as most anticancer treatments are based on DNA damaging agents, the regulatory function of Akt in DNA repair mechanisms contributes significantly to the resistance of tumors to cancer therapy. Therefore, a Special Issue of IJMS (with Guest Editor H. Peter Rodemann, Tübingen, and Ekkehard Dikomey, Hamburg) is planned, publishing the most current research findings on various topics related to Akt and its role in DNA damage response, in the form of both original as well as review articles, in 2020.

Prof. Dr. H. Peter Rodemann
Prof. Dr. Ekkehard Dikomey
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • Akt signaling
  • DNA damage response pathways
  • Resistance of tumor cells to genotoxic therapies

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Published Papers (2 papers)

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Review

33 pages, 3812 KiB  
Review
A New Twist in Protein Kinase B/Akt Signaling: Role of Altered Cancer Cell Metabolism in Akt-Mediated Therapy Resistance
by Isabell Götting, Verena Jendrossek and Johann Matschke
Int. J. Mol. Sci. 2020, 21(22), 8563; https://doi.org/10.3390/ijms21228563 - 13 Nov 2020
Cited by 19 | Viewed by 4707
Abstract
Cancer resistance to chemotherapy, radiotherapy and molecular-targeted agents is a major obstacle to successful cancer therapy. Herein, aberrant activation of the phosphatidyl-inositol-3-kinase (PI3K)/protein kinase B (Akt) pathway is one of the most frequently deregulated pathways in cancer cells and has been associated with [...] Read more.
Cancer resistance to chemotherapy, radiotherapy and molecular-targeted agents is a major obstacle to successful cancer therapy. Herein, aberrant activation of the phosphatidyl-inositol-3-kinase (PI3K)/protein kinase B (Akt) pathway is one of the most frequently deregulated pathways in cancer cells and has been associated with multiple aspects of therapy resistance. These include, for example, survival under stress conditions, apoptosis resistance, activation of the cellular response to DNA damage and repair of radiation-induced or chemotherapy-induced DNA damage, particularly DNA double strand breaks (DSB). One further important, yet not much investigated aspect of Akt-dependent signaling is the regulation of cell metabolism. In fact, many Akt target proteins are part of or involved in the regulation of metabolic pathways. Furthermore, recent studies revealed the importance of certain metabolites for protection against therapy-induced cell stress and the repair of therapy-induced DNA damage. Thus far, the likely interaction between deregulated activation of Akt, altered cancer metabolism and therapy resistance is not yet well understood. The present review describes the documented interactions between Akt, its target proteins and cancer cell metabolism, focusing on antioxidant defense and DSB repair. Furthermore, the review highlights potential connections between deregulated Akt, cancer cell metabolism and therapy resistance of cancer cells through altered DSB repair and discusses potential resulting therapeutic implications. Full article
(This article belongs to the Special Issue Akt and Its Role in DNA Damage Response (DDR) Pathways)
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21 pages, 1725 KiB  
Review
SOX2 and p53 Expression Control Converges in PI3K/AKT Signaling with Versatile Implications for Stemness and Cancer
by Thorsten Schaefer, Rebekah Steiner and Claudia Lengerke
Int. J. Mol. Sci. 2020, 21(14), 4902; https://doi.org/10.3390/ijms21144902 - 11 Jul 2020
Cited by 24 | Viewed by 6999
Abstract
Stemness and reprogramming involve transcriptional master regulators that suppress cell differentiation while promoting self-renewal. A distinguished example thereof is SOX2, a high mobility group (HMG)-box transcription factor (TF), whose subcellular localization and turnover regulation in embryonic, induced-pluripotent, and cancer stem cells (ESCs, iPSCs, [...] Read more.
Stemness and reprogramming involve transcriptional master regulators that suppress cell differentiation while promoting self-renewal. A distinguished example thereof is SOX2, a high mobility group (HMG)-box transcription factor (TF), whose subcellular localization and turnover regulation in embryonic, induced-pluripotent, and cancer stem cells (ESCs, iPSCs, and CSCs, respectively) is mediated by the PI3K/AKT/SOX2 axis, a stem cell-specific branch of the PI3K/AKT signaling pathway. Further effector functions associated with PI3K/AKT induction include cell cycle progression, cellular (mass) growth, and the suppression of apoptosis. Apoptosis, however, is a central element of DNA damage response (DDR), where it provides a default mechanism for cell clearance when DNA integrity cannot be maintained. A key player in DDR is tumor suppressor p53, which accumulates upon DNA-damage and is counter-balanced by PI3K/AKT enforced turnover. Accordingly, stemness sustaining SOX2 expression and p53-dependent DDR mechanisms show molecular–functional overlap in PI3K/AKT signaling. This constellation proves challenging for stem cells whose genomic integrity is a functional imperative for normative ontogenesis. Unresolved mutations in stem and early progenitor cells may in fact provoke transformation and cancer development. Such mechanisms are also particularly relevant for iPSCs, where genetic changes imposed through somatic cell reprogramming may promote DNA damage. The current review aims to summarize the latest advances in the understanding of PI3K/AKT/SOX2-driven stemness and its intertwined relations to p53-signaling in DDR under conditions of pluripotency, reprogramming, and transformation. Full article
(This article belongs to the Special Issue Akt and Its Role in DNA Damage Response (DDR) Pathways)
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