p53 Pathway in Cancer Progression and Cancer Therapy

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

Deadline for manuscript submissions: closed (26 January 2018) | Viewed by 11472

Special Issue Editor

Institute of Molecular Genetics, Prague, Czech Republic
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

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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

18 pages, 932 KiB  
Review
p53-Mediated Molecular Control of Autophagy in Tumor Cells
by Maria Mrakovcic and Leopold F. Fröhlich
Biomolecules 2018, 8(2), 14; https://doi.org/10.3390/biom8020014 - 21 Mar 2018
Cited by 127 | Viewed by 10994
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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