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Cells
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Cancer-Associated Fibroblasts: Challenges and Directions—Second Edition
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Cancer-Associated Fibroblasts: Challenges and Directions—Second Edition

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Microenvironment".

Deadline for manuscript submissions: 20 September 2026 | Viewed by 901

Editors

Dr. Paul J. Higgins

E-Mail Website
Guest Editor
Department of Regenerative and Cancer Cell Biology, Albany Medical College, 47 New Scotland Avenue, Albany, NY 12208-3479, USA
Interests: tumor microenvironment; tissue fibrosis; desmoplastic cancers; SERPINE1; transcriptomics/proteomics
Special Issues, Collections and Topics in MDPI journals
Dr. Ramesh Mukkamala

E-Mail Website
Guest Editor
Department of Chemistry, Purdue University, West Lafayette, IN 47907, USA
Interests: design and development of targeted ligands and drugs; molecular imaging; preclinical development of FAP-targeted radioligands
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cancer-associated fibroblasts (CAFs) represent a significant cellular component within the tumor microenvironment (TME) and play a crucial role in facilitating tumor growth. They directly contribute to tumor progression by releasing various growth factors, including vascular endothelial growth factor (VEGF), platelet-derived growth factor (PDGF), fibroblast growth factor (FGF), and various chemokines that stimulate angiogenesis and promote tumor development. Additionally, CAFs indirectly support tumor growth by secreting immune-suppressive cytokines like TGF-β, IL-8, and IL-10, and by remodeling the extracellular matrix (ECM), thereby rendering tumors resistant to various therapeutic interventions.

Cancer-associated fibroblasts (CAFs) are identified through several biomarkers, including α-SMA, PDGFRα/β, and fibroblast activation protein alpha (FAPα), among others. Notably, recent interest has grown around the reprogramming of the tumor microenvironment through the use of FAP-targeting ligand conjugates. This approach has gained prominence due to the exclusive overexpression of FAP in CAFs, with minimal to undetectable expression in healthy tissues. Currently, there are ongoing developments in the clinical use of 68Ga/177Lu-labeled FAP-targeting small molecules and peptide-based PET imaging agents, as well as radiotherapeutic agents.

This Special Issue will focus on original preclinical studies or comprehensive review articles. Topics can include the methods used to target CAF directly or indirectly until depletion of CAFs or elimination of tumor promotion, as well as the immunosuppressive function of CAFs using a combination of different therapeutic strategies for cancer treatment.

Dr. Paul J. Higgins
Dr. Ramesh Mukkamala
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 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-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells 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 2700 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

  • cancer-associated fibroblast (CAFs)
  • tumor microenvironment (TME)
  • fibroblast activation protein alpha (FAPα)
  • immunotherapy
  • cytokines
  • angiogenesis
  • metastasis
  • FAP inhibitors
  • radioligands
  • imaging agents

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Published Papers (1 paper)

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Research

17 pages, 15634 KB  
Communication
Mechanical Stiffening Promotes Growth, Invasion-Associated Phenotypes, and Reduced Selumetinib Sensitivity in 3D Plexiform Neurofibroma Cultures
by Kyungmin Ji, Chenjun Shi, Jitao Zhang and Raymond R. Mattingly
Cells 2026, 15(10), 877; https://doi.org/10.3390/cells15100877 - 12 May 2026
Viewed by 602
Abstract
Plexiform neurofibromas (pNF1s) are benign peripheral nerve sheath tumors caused by NF1 loss, leading to dysregulated RAS/mitogen-activated protein kinase (MAPK) signaling. While the mitogen-activated protein kinase kinase (MEK) inhibitors, selumetinib and mirdametinib, can reduce tumor volume, surgical resection remains the primary treatment for [...] Read more.
Plexiform neurofibromas (pNF1s) are benign peripheral nerve sheath tumors caused by NF1 loss, leading to dysregulated RAS/mitogen-activated protein kinase (MAPK) signaling. While the mitogen-activated protein kinase kinase (MEK) inhibitors, selumetinib and mirdametinib, can reduce tumor volume, surgical resection remains the primary treatment for immediate debulking and symptom relief. Complete removal is often limited by tumor infiltration along nerve plexuses, and residual tumors may undergo postsurgical tissue remodeling, producing localized regions of stiffened extracellular matrix (ECM). The impact of ECM stiffness on pNF1 growth and drug responses remains unclear. Using immortalized patient-derived pNF1 tumor cell lines cultured in 3D hydrogels with defined stiffness (1.5 kPa, soft; 7 kPa, stiff), we found that stiff ECM promoted spread morphology, increased growth, and progressive intracellular softening. Stiff ECM also reduced lysyl oxidase (LOX) expression, suggesting mechanoadaptive ECM remodeling, and increased P-glycoprotein expression. Under the same conditions, stiff ECM was associated with reduced sensitivity to selumetinib. These results provide the first evidence that ECM stiffening, including that plausibly associated with postsurgical remodeling, may contribute to pNF1 growth and reduced sensitivity to selumetinib in this 3D pNF1 culture model. Our findings highlight mechanobiology as a key regulator of tumor behavior and support further investigation of ECM-targeted strategies to improve outcomes in neurofibromatosis type 1 (NF1). Full article
(This article belongs to the Special Issue Cancer-Associated Fibroblasts: Challenges and Directions—Second Edition)
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