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Cell Cycle Dysregulation in Cancers

This special issue belongs to the section “Molecular Cancer Biology“.

Special Issue Information

Dear Colleagues,

The decision of a cell to proliferate or to enter a non-proliferative state is fundamental to multicellular homeostasis and is tightly governed by cell cycle checkpoints that integrate both cell-intrinsic programs and extrinsic cues from the tumor microenvironment. Nutrient availability, hypoxia, mechanical forces, inflammatory signals, and therapeutic stress continuously shape cell cycle progression, quiescence, and senescence, thereby influencing cancer evolution and treatment response. Rather than existing as discrete proliferative or non-proliferative categories, cell cycle states are now understood as a dynamic continuum, encompassing rapidly proliferating, slow-cycling, quiescent (shallow and deep), and senescent states. Importantly, even senescence—long considered a uniform and irreversible condition—is increasingly recognized as heterogeneous and potentially reversible, particularly in the context of microenvironmental signaling.

While the core cell cycle machinery, including cyclins, cyclin-dependent kinases (CDKs), and CDK inhibitors, has been extensively characterized, additional regulatory layers upstream of these components fine-tune cell cycle decisions in response to environmental inputs. These layers include kinases, phosphatases, acetyltransferases, methyltransferases, and ubiquitin and SUMO ligases that dynamically sense microenvironmental and stress-associated signals to regulate cell cycle progression and the depth and stability of cell cycle arrest. Dysregulation of these networks promotes cancer initiation and progression and enables therapeutic resistance, as checkpoints that normally constrain proliferation are repurposed to support cancer cell survival under hostile microenvironmental and treatment-induced conditions.

This Special Issue aims to capture novel insights into cell cycle deregulation across cancer progression, with a particular emphasis on the influence of the tumor microenvironment and environmental stress adaptation. It welcomes basic, translational, and clinical research articles, as well as original and insightful reviews, addressing mechanisms of cell cycle control, tumor–microenvironment interactions, and therapeutic strategies targeting cell cycle regulation to overcome cancer resistance.

Dr. Radoslav Janostiak
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 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 communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

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. Cancers 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 2900 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

  • cell cycle regulation
  • proliferation-quiescence decision
  • post translational regulation
  • quiescence maintenance
  • senescence escape
  • environmental stress adaptation
  • minimal residual disease
  • cell cycle checkpoints

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Cancers - ISSN 2072-6694