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Cells
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Signaling Pathways and Personalized Therapy in Cancer
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Signaling Pathways and Personalized Therapy in Cancer

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

Deadline for manuscript submissions: closed (15 May 2023) | Viewed by 2192

Special Issue Editor

Dr. Leonard Girnita

E-Mail Website
Guest Editor
1. Department of Oncology-Pathology, Cellular and Molecular Tumor Pathology, Karolinska Institute, 17164 Stockholm, Sweden
2. Karolinska University Hospital, Solna, Sweden
Interests: signaling; RTK; GPCR; ubiquitination; cancer; arrestin; GRK; IGF-1R; targeted therapy insulin; Insulin/IGF axis; metabolic syndrome; molecular pathology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The cellular signaling field has borne witness to multiple paradigm shifts that have important ramifications in our understanding of important physiological processes such as growth, differentiation and aging. Equally importantly, cell signaling anomalies play a dominant role in disease development, including diabetes and cancer. These abnormal signals are often initiated or sustained by plasma membrane receptors, such as tyrosine–kinase receptors (RTK), G protein-coupled receptors (GPCRs), and/or by their intracellular messengers. Different receptor families can utilize common intracellular signaling proteins and pathways; however, biological outcomes are canonically assigned to one or another cell surface receptor family. This multilayered crosstalk between different receptor families controlling the biological outcomes is insufficiently explored or considered for personalized medicine.

This Special Issue of Cells will follow the development of our understanding of cellular signaling pathology, as well as the design of targeted therapy controlling plasma-membrane receptors and their signaling network, with a particular focus on those relating to cancer or metabolic disorders.

Dr. Leonard Girnita
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

  • RTKs
  • GPCR
  • precision medicine
  • biomarkers
  • arrestin
  • ubiquitination

Published Papers (1 paper)

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Research

16 pages, 5612 KiB  
Article
A Non-Canonical Role for the Glycosyltransferase Enzyme UGT2B17 as a Novel Constituent of the B Cell Receptor Signalosome
by Antoine Wagner, Michèle Rouleau, Lyne Villeneuve, Trang Le, Cheryl Peltier, Éric P. Allain, Caroline Beaudoin, Sophie Tremblay, Fréderic Courtier, Flora Nguyen Van Long, Isabelle Laverdière, Éric Lévesque, Versha Banerji, Katrina Vanura and Chantal Guillemette
Cells 2023, 12(9), 1295; https://doi.org/10.3390/cells12091295 - 2 May 2023
Cited by 1 | Viewed by 1879
Abstract
In chronic lymphocytic leukemia (CLL), an elevated glycosyltransferase UGT2B17 expression (UGT2B17HI) identifies a subgroup of patients with shorter survival and poor drug response. We uncovered a mechanism, possibly independent of its enzymatic function, characterized by an enhanced expression and signaling of [...] Read more.
In chronic lymphocytic leukemia (CLL), an elevated glycosyltransferase UGT2B17 expression (UGT2B17HI) identifies a subgroup of patients with shorter survival and poor drug response. We uncovered a mechanism, possibly independent of its enzymatic function, characterized by an enhanced expression and signaling of the proximal effectors of the pro-survival B cell receptor (BCR) pathway and elevated Bruton tyrosine kinase (BTK) phosphorylation in B-CLL cells from UGT2B17HI patients. A prominent feature of B-CLL cells is the strong correlation of UGT2B17 expression with the adverse marker ZAP70 encoding a tyrosine kinase that promotes B-CLL cell survival. Their combined high expression levels in the treatment of naïve patients further defined a prognostic group with the highest risk of poor survival. In leukemic cells, UGT2B17 knockout and repression of ZAP70 reduced proliferation, suggesting that the function of UGT2B17 might involve ZAP70. Mechanistically, UGT2B17 interacted with several kinases of the BCR pathway, including ZAP70, SYK, and BTK, revealing a potential therapeutic vulnerability. The dual SYK and JAK/STAT6 inhibitor cerdulatinib most effectively compromised the proliferative advantage conferred by UGT2B17 compared to the selective BTK inhibitor ibrutinib. Findings point to an oncogenic role for UGT2B17 as a novel constituent of BCR signalosome also connected with microenvironmental signaling. Full article
(This article belongs to the Special Issue Signaling Pathways and Personalized Therapy in Cancer)
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