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Signalling Pathways in Metabolic Diseases and Cancers

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: 20 June 2025 | Viewed by 382

Special Issue Editor


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Guest Editor
Department of Experimental and Clinical Medicine, University “Magna Graecia” Catanzaro, 88100 Catanzaro, Italy
Interests: molecular biology; cancer; cell line; cell culture; flow cytometry analysis; Western blotting; gene expression; sequencing; proteomics; seminoma cell line; prostate cancer cell lines
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Special Issue Information

Dear Colleagues,

Cellular signaling pathways play a crucial role in cellular communication and adaptation to the everchanging surrounding environment, ultimately governing key fate decisions such as cell death, survival, division, or senescence. Cellular signaling processes are elicited by a variety of extracellular and intracellular inducers, such as growth factors, nutrients, or stress and damage stimuli. Likewise, the transmission of information on activated signaling pathways can rely on a plethora of signaling mediators. Moreover, many of these pathways are connected to form signaling networks to ensure the right timing and termination of cell responses. Notably, the dysregulation of signaling pathways has been implicated in the pathogenesis of several diseases, including cancer, inflammation, and metabolic disorders.

We therefore welcome original papers that report novel research findings and results on different aspects of cellular signaling, with special attention paid to novel regulators of pro-survival/pro-apoptotic signaling cascades; advances in targeted therapeutic strategies to manipulate signaling cascades, such as immunological therapies and so on; and the investigation of dysregulated molecular mechanisms underlying several metabolic and immunological diseases and tumors.

This Special Issue is supervised by Dr. Bossio and assisted by Dr. Gallo and Dr. Palummo.

Dr. Sabrina Bossio
Guest Editor

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Keywords

  • cancer
  • prostate cancer
  • molecular signalling pathway
  • metabolic diseases
  • diabets
  • immunotherapy
  • immunological diseases

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Published Papers (1 paper)

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Research

15 pages, 3257 KiB  
Article
Inhibiting the TGF-β1 Pathway Reduces the Aggressiveness of Intrahepatic CCA HuCCT1 CD90-Positive Cells
by Elena Pizzuto, Serena Mancarella, Isabella Gigante, Grazia Serino, Francesco Dituri, Emanuele Piccinno, Isabel Fabregat and Gianluigi Giannelli
Int. J. Mol. Sci. 2025, 26(11), 4973; https://doi.org/10.3390/ijms26114973 - 22 May 2025
Abstract
Molecular mechanisms responsible for the poor prognosis in patients with intrahepatic cholangiocarcinoma (CCA) are still unknown, but stem cell marker Cluster Differentiation 90 (CD90) has been reported to be associated with a more aggressive cancer phenotype. In this scenario, the TGF-β1 signaling pathway [...] Read more.
Molecular mechanisms responsible for the poor prognosis in patients with intrahepatic cholangiocarcinoma (CCA) are still unknown, but stem cell marker Cluster Differentiation 90 (CD90) has been reported to be associated with a more aggressive cancer phenotype. In this scenario, the TGF-β1 signaling pathway likely has a role as master gene regulator. Aim of the study is to investigate the role of CD90 in iCCA aggressiveness. The molecular profile of HuCCT1/CD90+ and HuCCT1/CD90− cells was obtained through transcriptomic analysis (NGS). Bioinformatic data were confirmed in both cell lines by qRT-PCR and Western blot. Cells were treated with Gemcitabine in monotherapy or in combination with Galunisertib, a selective inhibitor of TGF-βRI, in 2D and 3D models. HuCCT1/CD90+ cells are more proliferative, less migratory, and resistant to Gemcitabine treatment. HuCCT1/CD90+ cells also express lower levels of TGF-β1 compared to /CD90− cell lines. Finally, HuCCT1/CD90+ cells are resistant to Gemcitabine, while the combination of Gemcitabine and Galunisertib displays a synergistic effect on HuCCT1/CD90+ cell proliferation. These results underline that CD90-induced Gemcitabine resistance can be overcome by adding a TGFβ1 inhibitor such as Galunisertib, thereby moving further toward a precision medicine approach in patients with iCCA. Full article
(This article belongs to the Special Issue Signalling Pathways in Metabolic Diseases and Cancers)
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