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Cells
Special Issues
New Insights of TGF-Beta Signaling in Cancer
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New Insights of TGF-Beta Signaling in Cancer

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

Deadline for manuscript submissions: closed (31 March 2025) | Viewed by 2095

Special Issue Editor

Prof. Dr. Hendrik Ungefroren

E-Mail Website
Guest Editor
1. First Department of Medicine, Campus Lübeck, University Hospital Schleswig-Holstein (UKSH), Ratzeburger Allee 160, 23538 Lübeck, Germany
2. Department of Surgery, Campus Lübeck, University Hospital Schleswig-Holstein (UKSH), Ratzeburger Allee 160, 23538 Lübeck, Germany
3. Institute of Pathology, Campus Kiel, University Hospital Schleswig-Holstein (UKSH), Arnold-Heller Str. 5, 24105 Kiel, Germany
Interests: TGF-beta signaling and its crosstalk with other signaling pathways; cell migration and invasion; mechanisms of metastasis; tumor biology; pancreatic tumors; small GTPases; neuroendocrine differentiation, epithelial–mesenchymal transition; mesenchymal–epithelial transititon
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Special Issue Information

Dear Colleagues,

Transforming the growth factor (TGF)-β plays a pivotal role in the control of different cellular processes, including proliferation, cell death, differentiation, and migration during both embryonic development and adulthood. Unsurprisingly, the dysregulation of its expression and the altered activation of its intracellular signaling pathways contribute to human diseases, such as tissue fibrosis and cancer. During tumorigenesis, TGF-β may have anticancer activity at early stages, mainly due to its strong antiproliferative effects; however, increasing evidence suggests that the mutational inactivation of the canonical Smad pathway with the concurrent overactivation of non-canonical Smad and non-Smad pathways could contribute to tumor progression at later stages, i.e., by favoring immune suppression, cell invasion, and metastasis. Authors are invited to submit manuscripts that show the possible alterations of these pathways and how they interact with each other in tumor cells. The data may provide useful information on how to better and more selectively target TGF-β signaling for inhibition in various types of human cancer with the goal to improve the prognosis of cancer patients.

In this Special Issue, we aim to shed light on the state-of-the-art and novel data that help to increase our knowledge on the role of TGF-β signaling in the development and progression of human cancer. We welcome experts in the field to contribute research papers and critical reviews on the various facets of TGF-β signaling that either suppress or promote cancer development, as well as on how natural and pharmacological pathway inhibitors for TGF-β signaling, may be exploited as tools in anti-cancer therapies.

Prof. Dr. Hendrik Ungefroren
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. 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
  • TGF-beta
  • signaling crosstalk
  • smad signaling, non-Smad signaling
  • TGF-beta receptors
  • TGF-beta signaling inhibitors
  • TGF-beta paradox
  • epithelial-mesenchymal transition (EMT)
  • mesenchymal-epithelial transition (MET)

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Published Papers (1 paper)

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Research

22 pages, 3450 KiB  
Article
Characterization of Epithelial–Mesenchymal and Neuroendocrine Differentiation States in Pancreatic and Small Cell Ovarian Tumor Cells and Their Modulation by TGF-β1 and BMP-7
by Hendrik Ungefroren, Juliane von der Ohe, Rüdiger Braun, Yola Gätje, Olha Lapshyna, Jörg Schrader, Hendrik Lehnert, Jens-Uwe Marquardt, Björn Konukiewitz and Ralf Hass
Cells 2024, 13(23), 2010; https://doi.org/10.3390/cells13232010 - 5 Dec 2024
Cited by 1 | Viewed by 1569
Abstract
Pancreatic ductal adenocarcinoma (PDAC) has an extremely poor prognosis, due in part to early invasion and metastasis, which in turn involves epithelial–mesenchymal transition (EMT) of the cancer cells. Prompted by the discovery that two PDAC cell lines of the quasi-mesenchymal subtype (PANC-1, MIA [...] Read more.
Pancreatic ductal adenocarcinoma (PDAC) has an extremely poor prognosis, due in part to early invasion and metastasis, which in turn involves epithelial–mesenchymal transition (EMT) of the cancer cells. Prompted by the discovery that two PDAC cell lines of the quasi-mesenchymal subtype (PANC-1, MIA PaCa-2) exhibit neuroendocrine differentiation (NED), we asked whether NED is associated with EMT. Using real-time PCR and immunoblotting, we initially verified endogenous expressions of various NED markers, i.e., chromogranin A (CHGA), synaptophysin (SYP), somatostatin receptor 2 (SSTR2), and SSTR5 in PANC-1 and MIA PaCa-2 cells. By means of immunohistochemistry, the expressions of CHGA, SYP, SSTR2, and the EMT markers cytokeratin 7 (CK7) and vimentin could be allocated to the neoplastic ductal epithelial cells of pancreatic ducts in surgically resected tissues from patients with PDAC. In HPDE6c7 normal pancreatic duct epithelial cells and in epithelial subtype BxPC-3 PDAC cells, the expression of CHGA, SYP, and neuron-specific enolase 2 (NSE) was either undetectable or much lower than in PANC-1 and MIA PaCa-2 cells. Parental cultures of PANC-1 cells exhibit EM plasticity (EMP) and harbor clonal subpopulations with both M- and E-phenotypes. Of note, M-type clones were found to display more pronounced NED than E-type clones. Inducing EMT in parental cultures of PANC-1 cells by treatment with transforming growth factor-β1 (TGF-β1) repressed epithelial genes and co-induced mesenchymal and NED genes, except for SSTR5. Surprisingly, treatment with bone morphogenetic protein (BMP)-7 differentially affected gene expressions in PANC-1, MIA PaCa-2, BxPC-3, and HPDE cells. It synergized with TGF-β1 in the induction of vimentin, SNAIL, SSTR2, and NSE but antagonized it in the regulation of CHGA and SSTR5. Phospho-immunoblotting in M- and E-type PANC-1 clones revealed that both TGF-β1 and, surprisingly, also BMP-7 activated SMAD2 and SMAD3 and that in M- but not E-type clones BMP-7 was able to dramatically enhance the activation of SMAD3. From these data, we conclude that in EMT of PDAC cells mesenchymal and NED markers are co-regulated, and that mesenchymal–epithelial transition (MET) is associated with a loss of both the mesenchymal and NED phenotypes. Analyzing NED in another tumor type, small cell carcinoma of the ovary hypercalcemic type (SCCOHT), revealed that two model cell lines of this disease (SCCOHT-1, BIN-67) do express CDH1, SNAI1, VIM, CHGA, SYP, ENO2, and SSTR2, but that in contrast to BMP-7, none of these genes was transcriptionally regulated by TGF-β1. Likewise, in BIN-67 cells, BMP-7 was able to reduce proliferation, while in SCCOHT-1 cells this occurred only upon combined treatment with TGF-β and BMP-7. We conclude that in PDAC-derived tumor cells, NED is closely linked to EMT and TGF-β signaling, which may have implications for the therapeutic use of TGF-β inhibitors in PDAC management. Full article
(This article belongs to the Special Issue New Insights of TGF-Beta Signaling in Cancer)
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