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Biomedicines
Special Issues
Advanced Research in Cell Motility 2.0
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Advanced Research in Cell Motility 2.0

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: closed (31 March 2023) | Viewed by 1600

Special Issue Editor

Dr. Daniel Zicha

E-Mail Website
Guest Editor
Central European Institute of Technology, Brno University of Technology, Brno, Czech Republic
Interests: cell motility; cancer metastasis; light microscopy; quantitative phase imaging

Special Issue Information

Dear Colleagues,

Since 1996, the number of publications on “cell motility” has increased four-fold in biomedical research, particularly in cell biology, oncology, and biochemistry molecular biology (Web of Science). This increased interest was mainly driven by the need to complement significant progress in molecular genetics as well emerging tools facilitating analysis in this field. The introduction of digital cameras into time-lapse light microscopy, live cell fluorescence labeling, and quantitative phase imaging has also led to more accurate cell motility measurements. This Special Issue will present an interdisciplinary research platform for research on molecular bases, pathology, and technologies in cell motility.

Dr. Daniel Zicha
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. Biomedicines is an international peer-reviewed open access monthly 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 2600 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

  • migration
  • chemotaxis
  • cell extension
  • cell retraction
  • quantitative phase imaging
  • time lapse

Published Papers (1 paper)

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Research

12 pages, 1741 KiB  
Article
Suppressive Role of ACVR1/ALK2 in Basal and TGFβ1-Induced Cell Migration in Pancreatic Ductal Adenocarcinoma Cells and Identification of a Self-Perpetuating Autoregulatory Loop Involving the Small GTPase RAC1b
by Hendrik Ungefroren, Rüdiger Braun, Olha Lapshyna, Björn Konukiewitz, Ulrich F. Wellner, Hendrik Lehnert and Jens-Uwe Marquardt
Biomedicines 2022, 10(10), 2640; https://doi.org/10.3390/biomedicines10102640 - 20 Oct 2022
Cited by 3 | Viewed by 1348
Abstract
Pancreatic ductal adenocarcinoma (PDAC) cells are known for their high invasive/metastatic potential, which is regulated in part by the transforming growth factor β1 (TGFβ1). The involvement of at least two type I receptors, ALK5 and ALK2, that transmit downstream signals of the TGFβ [...] Read more.
Pancreatic ductal adenocarcinoma (PDAC) cells are known for their high invasive/metastatic potential, which is regulated in part by the transforming growth factor β1 (TGFβ1). The involvement of at least two type I receptors, ALK5 and ALK2, that transmit downstream signals of the TGFβ via different Smad proteins, SMAD2/3 and SMAD1/5, respectively, poses the issue of their relative contribution in regulating cell motility. Real-time cell migration assays revealed that the selective inhibition of ALK2 by RNAi or dominant-negative interference with a kinase-dead mutant (ALK2-K233R) strongly enhanced the cells’ migratory activity in the absence or presence of TGFβ1 stimulation. Ectopic ALK2-K233R expression was associated with an increase in the protein levels of RAC1 and its alternatively spliced isoform, RAC1b, both of which are implicated in driving cell migration and invasion. Conversely, the RNAi-mediated knockdown or CRISPR/Cas9-mediated knockout of RAC1b resulted in the upregulation of the expression of ALK2, but not that of the related BMP type I receptors, ALK3 or ALK6, and elevated the phosphorylation of SMAD1/5. PDAC is a heterogeneous disease encompassing tumors with different histomorphological subtypes, ranging from epithelial/classical to extremely mesenchymal. Upon treatment of various established and primary PDAC cell lines representing these subtypes with the ALK2 inhibitor, LDN-193189, well-differentiated, epithelial cell lines responded with a much stronger increase in the basal and TGFβ1-dependent migratory activity than poorly differentiated, mesenchymal ones. These data show that (i) ALK2 inhibits migration by suppressing RAC1/RAC1b proteins, (ii) ALK2 and RAC1b act together in a self-perpetuating the autoregulatory negative feedback loop to mutually control their expression, and (iii) the ALK2 antimigratory function appears to be particularly crucial in protecting epithelial subtype cells from becoming invasive, both spontaneously and in a TGFβ-rich tumor microenvironment. Full article
(This article belongs to the Special Issue Advanced Research in Cell Motility 2.0)
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