Special Issue "The Role of the Cytoskeleton in Tumor Progression"

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Cancer Pathophysiology".

Deadline for manuscript submissions: 31 May 2024 | Viewed by 1571

Special Issue Editor

Department of Cell and Cancer Biology, University of Toledo College of Medicine, Toledo, OH 43614, USA
Interests: cytoskeleton effector proteins; glioblastoma invasion

Special Issue Information

Dear Colleagues,

The cytoskeleton is an organized, dynamic meshwork of protein filaments that reinforce cell membranes, provide cell shape and structural integrity, and facilitate essential cellular functions. The eukaryotic cytoskeleton is composed of three classes of filamentous fibers: actin filaments, intermediate filaments, and microtubules. Cells utilize a dynamic cytoskeleton to generate force that propels them into and through the extracellular space. Cytoskeletal filament polymerization and/or tractional tension generated against existing filaments provides that force. Differences in ECM adhesions, actin protrusions, and actomyosin contractility characterize cellular motility patterns (i.e., amoeboid, collective, mesenchymal motility). These features are dictated by differences in gene expression, signaling activity, and environmental factors.

Loss of control over cellular motility pathways is a central feature of malignancy. Dynamic remodeling of both the actin and microtubule cytoskeletal systems is required for microstructural and macrostructural patterns for tumor cell invasion. Understanding the contributions of mechanisms underlying dynamic cytoskeleton remodeling in motile cancer cells will support generation of therapeutics targeting cancer cell motility to aid in the control of tumor progression. This Special Issue seeks to highlight the current state of the art in basic and (pre)clinical cytoskeleton research in tumor cell motility, including understanding the formation of pro-invasion cytoskeletal structures (e.g., invadopodia, tumor microtubes, or tunneling nanotubes, amongst others) which may contribute to therapeutic resistance and disease progression.

Prof. Dr. Kathryn M. Eisenmann
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 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. 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.


  • cytoskeleton
  • actin
  • tubulin
  • invasion
  • metastasis
  • Rho GTPase
  • tumor microtube
  • tunneling nanotube
  • targeted therapy
  • tumor progression

Published Papers (1 paper)

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26 pages, 3590 KiB  
MCAK Inhibitors Induce Aneuploidy in Triple-Negative Breast Cancer Models
Cancers 2023, 15(13), 3309; https://doi.org/10.3390/cancers15133309 - 23 Jun 2023
Cited by 1 | Viewed by 1413
Standard of care for triple-negative breast cancer (TNBC) involves the use of microtubule poisons such as paclitaxel, which are proposed to work by inducing lethal levels of aneuploidy in tumor cells. While these drugs are initially effective in treating cancer, dose-limiting peripheral neuropathies [...] Read more.
Standard of care for triple-negative breast cancer (TNBC) involves the use of microtubule poisons such as paclitaxel, which are proposed to work by inducing lethal levels of aneuploidy in tumor cells. While these drugs are initially effective in treating cancer, dose-limiting peripheral neuropathies are common. Unfortunately, patients often relapse with drug-resistant tumors. Identifying agents against targets that limit aneuploidy may be a valuable approach for therapeutic development. One potential target is the microtubule depolymerizing kinesin, MCAK, which limits aneuploidy by regulating microtubule dynamics during mitosis. Using publicly available datasets, we found that MCAK is upregulated in triple-negative breast cancer and is associated with poorer prognoses. Knockdown of MCAK in tumor-derived cell lines caused a two- to five-fold reduction in the IC50 for paclitaxel, without affecting normal cells. Using FRET and image-based assays, we screened compounds from the ChemBridge 50 k library and discovered three putative MCAK inhibitors. These compounds reproduced the aneuploidy-inducing phenotype of MCAK loss, reduced clonogenic survival of TNBC cells regardless of taxane-resistance, and the most potent of the three, C4, sensitized TNBC cells to paclitaxel. Collectively, our work shows promise that MCAK may serve as both a biomarker of prognosis and as a therapeutic target. Full article
(This article belongs to the Special Issue The Role of the Cytoskeleton in Tumor Progression)
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