ijms-logo

Journal Browser

Journal Browser

Beyond Drivers and Suppressors: Investigating Upstream Regulators of Cell Death

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: 20 September 2026 | Viewed by 1263

Special Issue Editor

Special Issue Information

Dear Colleagues,

Regulated cell death (RCD) encompasses both well-characterized modalities (e.g., apoptosis, necroptosis, pyroptosis) and emerging forms such as ferroptosis, oxeiptosis, and alkaliptosis. This Special Issue invites studies elucidating the upstream control layers that prime, initiate, or tune these death programs. We welcome research mapping receptor–ligand and kinase circuits, metabolic and redox checkpoints, ion and pH homeostasis, non-coding RNAs, and transcriptional or epigenetic programs, as well as context dependence (cell type, microenvironment, infection) and cross-talk among RCD pathways. Submissions centered on classical cell-death modalities are fully in scope when they probe higher-order regulation or reveal new interfaces between pathways. 

The present Special Issue invites research expanding what is known about RCD axes, but, more importantly, it prioritizes studies that uncover previously unrecognized relationships. Because upstream regulation can shape cell death outcomes independently of pathway components (e.g., via epigenetic reprogramming, altered transcription factor networks, or metabolic rewiring), such studies are especially valued. We welcome original contributions in the form of in silico, in vitro, and in vivo investigations. Exploratory and bioinformatics-based analyses are encouraged when they propose conceptually novel relationships or testable hypotheses, as well as utilize rigorous scoring frameworks or pathway-activity metrics. Papers that fall outside these themes will also be evaluated.

This Special Issue is supervised by Dr. Damian Kołat and assisted by Dr. Elżbieta Płuciennik,  (Department of Functional Genomics, Medical University of Lodz, 90-752 Lodz, Poland) and Dr. Żaneta Kałuzińska-Kołat,  (Department of Biomedicine and Experimental Surgery, Medical University of Lodz, 90-136 Lodz, Poland). 

Dr. Damian Kołat
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 short 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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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 death
  • driver genes
  • suppressor genes
  • upstream regulators
  • gene expression
  • in silico
  • in vitro
  • in vivo

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Research

22 pages, 7647 KB  
Article
AP-2 Transcription Factors as Regulators of Ferroptosis: A Family-Wide Profiling in Diverse Cancer Contexts
by Damian Kołat, Piotr Gromek, Mateusz Kciuk, Lin-Yong Zhao, Żaneta Kałuzińska-Kołat, Renata Kontek and Elżbieta Płuciennik
Int. J. Mol. Sci. 2026, 27(5), 2310; https://doi.org/10.3390/ijms27052310 - 28 Feb 2026
Cited by 1 | Viewed by 657
Abstract
Ferroptosis is an iron-dependent programmed cell death (PCD) implicated in cancer therapy response, yet its transcriptional control remains unevenly characterized and often centered on a limited subset of transcription factors (TFs) rather than systematically addressing TF families. The Activating enhancer-binding Protein-2 (AP-2) family [...] Read more.
Ferroptosis is an iron-dependent programmed cell death (PCD) implicated in cancer therapy response, yet its transcriptional control remains unevenly characterized and often centered on a limited subset of transcription factors (TFs) rather than systematically addressing TF families. The Activating enhancer-binding Protein-2 (AP-2) family of TFs is a plausible but understudied regulatory node linking oncogenic programs to ferroptosis, with prior research limited to AP-2α and AP-2γ, suggesting anti-ferroptotic and pro-tumorigenic roles. Thus, the present study aimed to provide a family-wide analysis of the relationships between AP-2 and ferroptosis across tumors in which this PCD type is considered biologically and clinically relevant. The research integrates ferroptosis gene modules with AP-2 targetomes, tumor–normal expression comparisons, survival stratification, ferroptosis scoring, cross-cohort functional analyses, and signaling pathway projection extending canonical ferroptosis circuits with AP-2–associated non-canonical elements. Consistent associations between AP-2 expression, prognosis, and ferroptosis score were observed in five tumor cohorts: cervical squamous cell carcinoma, glioblastoma, ovarian serous cystadenocarcinoma, pancreatic adenocarcinoma, and thyroid carcinoma. In addition, cross-cohort clustering highlighted genes enriched in redox- and lipid-metabolism programs linked to apoptosis and autophagy-dependent death. Among the candidates emerging from these analyses, ferroptotic markers (LOX, PTGS2, and NQO1) and AP-2–linked nodes such as CD36, DUOX1, EPHA2, MUC1, PTPRC, SNAI2, and TP63 warrant targeted functional and binding validation to infer whether these associations reflect direct AP-2 regulatory mechanisms. Most importantly, AP-2–centered research appears to be a valuable area for guiding studies of tumor-specific ferroptosis vulnerability or resistance. Full article
Show Figures

Figure 1

Back to TopTop