Special Issue "p53 Pathway in Cancer Progression and Cancer Therapy"

A special issue of Biomolecules (ISSN 2218-273X).

Deadline for manuscript submissions: closed (26 January 2018)

Special Issue Editor

Guest Editor
Dr. Libor Macurek

Institute of Molecular Genetics, Prague, Czech Republic
Website | E-Mail
Interests: cell cycle checkpoint; DNA damage response; cancer

Special Issue Information

Dear Colleagues,

Mutation or functional inactivation of the tumor suppressor p53 promotes cancer development; therefore, p53 has been at the center of researchers’ interest for nearly four decades. Various stress response pathways converge on p53, which, by triggering transcription of target genes, controls essential cell fate decisions, ranging from a temporal cell cycle arrest to permanent senescence or apoptosis. In addition to these canonical roles, p53 is implicated in a plethora of other functions, including DNA repair, miRNA production, autophagy, energy metabolism, and stem cell differentiation. There is now emerging evidence that deficient p53 response, not only contributes to tumorigenesis, but could be also exploited in targeted cancer therapy. It has been shown that loss of p53 in cancer cells shows synthetic lethality with certain forms of chemotherapy. Discovery that p53 reactivation leads to tumor regression in animal models boosted the development of several small molecule antagonists of MDM2, which allow p53 stabilization and the induction of cell death in p53 proficient tumors. Finally, gain-of-function mutations of p53 promote stemness of cancer stem cells and, therefore, specific targeting of the mutant p53 could prevent tumor progression.

We encourage scientists to submit their original work or review articles focused on the novel roles of p53 in cell physiology and cancer development, or on the exploitation of p53 pathway in cancer therapy. Both translational and basic research papers are welcome.

Dr. Libor Macurek
Guest Editor

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 papers will be 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. Biomolecules is an international peer-reviewed open access quarterly 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 650 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

  • p53
  • cancer
  • tumor suppressor
  • DNA damage response
  • Cell cycle checkpoint
  • small-molecule inhibitor
  • cell death
  • synthetic lethality

Published Papers (1 paper)

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Review

Open AccessReview p53-Mediated Molecular Control of Autophagy in Tumor Cells
Biomolecules 2018, 8(2), 14; https://doi.org/10.3390/biom8020014
Received: 12 February 2018 / Revised: 16 March 2018 / Accepted: 19 March 2018 / Published: 21 March 2018
Cited by 3 | PDF Full-text (932 KB) | HTML Full-text | XML Full-text
Abstract
Autophagy is an indispensable mechanism of the eukaryotic cell, facilitating the removal and renewal of cellular components and thereby balancing the cell’s energy consumption and homeostasis. Deregulation of autophagy is now regarded as one of the characteristic key features contributing to the development
[...] Read more.
Autophagy is an indispensable mechanism of the eukaryotic cell, facilitating the removal and renewal of cellular components and thereby balancing the cell’s energy consumption and homeostasis. Deregulation of autophagy is now regarded as one of the characteristic key features contributing to the development of tumors. In recent years, the suppression of autophagy in combination with chemotherapeutic treatment has been approached as a novel therapy in cancer treatment. However, depending on the type of cancer and context, interference with the autophagic machinery can either promote or disrupt tumorigenesis. Therefore, disclosure of the major signaling pathways that regulate autophagy and control tumorigenesis is crucial. To date, several tumor suppressor proteins and oncogenes have emerged as eminent regulators of autophagy whose depletion or mutation favor tumor formation. The mammalian cell “janitor” p53 belongs to one of these tumor suppressors that are most commonly mutated in human tumors. Experimental evidence over the last decade convincingly reports that p53 can act as either an activator or an inhibitor of autophagy depending on its subcellular localization and its mode of action. This finding gains particular significance as p53 deficiency or mutant variants of p53 that accumulate in the cytoplasm of tumor cells enable activation of autophagy. Accordingly, we recently identified p53 as a molecular hub that regulates autophagy and apoptosis in histone deacetylase inhibitor-treated uterine sarcoma cells. In light of this novel experimental evidence, in this review, we focus on p53 signaling as a mediator of the autophagic pathway in tumor cells. Full article
(This article belongs to the Special Issue p53 Pathway in Cancer Progression and Cancer Therapy)
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