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Protein Kinases and Pseudokinases in Cancer and the Tumour Microenvironment

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

Deadline for manuscript submissions: closed (15 January 2024) | Viewed by 2486

Special Issue Editors


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Guest Editor
Department of Biochemistry and Biomedicine, School of Life Sciences, University of Sussex, Falmer, Brighton BN1 9QG, UK
Interests: cancer; tumour microenvironment; signal transduction; kinases; pseudokinases; fibroblasts; immune cells
Special Issues, Collections and Topics in MDPI journals

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Guest Editor
Section of Cell Biology & Biophysics, Department of Biology, School of Science, National and Kapodistrian University of Athens (NKUA), Panepistimiopolis, Zografou, 15701 Athens, Greece
Interests: development; cancer; chemotherapy; metastasis; programmed cell death; metabolism; Drosophila aging; brain signaling; proteasome
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We are pleased to announce the special issue: Protein Kinases and Pseudokinases in Cancer and the Tumour Microenvironment.

Protein kinases have a central role in cancer development and progression and represent excellent therapeutic targets. From early research to novel members of the human kinome, understanding of their contribution to diseases including cancer is growing every day. Moreover, it is also well-established that protein kinases play an important part in signalling within the tumour microenvironment.

Similar to their catalytically active counterparts, psuedokinases are essential component of the human kinome. With their unique structural features, the role of pseudokinases in a number of physiological processes and in human diseases has become increasingly apparent. Yet, members of the ‘pseudokinome’ remain largely unexplored.

This Special Issue aims to collect high-quality publications on the role of kinases and pseudokinases in both the development of cancer and their contribution within the tumour microenvironment. Original research papers and updated review articles are invited on topics including but not limited to: kinase and pseudokinase signalling in cancer initiation and progression and how these may be targeted in cancer treatments. Papers discussing the role of protein kinases in the tumour microenvironment and their involvment in interplay between the microenvrionment (eg. immune cells, fibroblasts, astrocytes, neuronal cells, etc) and cancer cells are also welcomed.

Prof. Dr. Georgios Giamas
Dr. Dimitrios J. Stravopodis
Guest Editors

Manuscript Submission Information

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Keywords

  • cancer
  • tumour microenvironment
  • signal transduction
  • kinases
  • pseudokinases
  • fibroblasts
  • immune cells
  • targeted therapy

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Published Papers (1 paper)

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Research

15 pages, 2205 KiB  
Article
Knockdown of PTK7 Reduces the Oncogenic Potential of Breast Cancer Cells by Impeding Receptor Tyrosine Kinase Signaling
by Won-Sik Shin, Si Won Oh, Han Na Park, Jae Hoon Kim and Seung-Taek Lee
Int. J. Mol. Sci. 2023, 24(15), 12173; https://doi.org/10.3390/ijms241512173 - 29 Jul 2023
Cited by 7 | Viewed by 1977
Abstract
Protein tyrosine kinase 7 (PTK7), a catalytically defective receptor tyrosine kinase (RTK), is often upregulated in various cancers. This study aimed to validate PTK7 as a target for breast cancer (BC) and investigate its oncogenic signaling mechanism. BC tissue analysis showed significantly elevated [...] Read more.
Protein tyrosine kinase 7 (PTK7), a catalytically defective receptor tyrosine kinase (RTK), is often upregulated in various cancers. This study aimed to validate PTK7 as a target for breast cancer (BC) and investigate its oncogenic signaling mechanism. BC tissue analysis showed significantly elevated PTK7 mRNA levels, especially in refractory triple-negative breast cancer (TNBC) tissues, compared with normal controls. Similarly, BC cell lines exhibited increased PTK7 expression. Knockdown of PTK7 inhibited the proliferation of T-47D and MCF-7 hormone-receptor-positive BC cell-lines and of HCC1187, MDA-MB-231, MDA-MB-436, and MDA-MB-453 TNBC cells. PTK7 knockdown also inhibited the adhesion, migration, and invasion of MDA-MB-231, MDA-MB-436, and MDA-MB-453 cells, and reduced the phosphorylation levels of crucial oncogenic regulators including extracellular signal-regulated kinase (ERK), Akt, and focal adhesion kinase (FAK). Furthermore, PTK7 interacts with fibroblast growth factor receptor 1 (FGFR1) and epidermal growth factor receptor (EGFR) expressed in MDA-MB-231 cells. Knockdown of PTK7 decreased the growth-factor-induced phosphorylation of FGFR1 and EGFR in MDA-MB-231 cells, indicating its association with RTK activation. In conclusion, PTK7 plays a significant role in oncogenic signal transduction by enhancing FGFR1 and EGFR activation, influencing BC tumorigenesis and metastasis. Hence, PTK7 represents a potential candidate for targeted BC therapy, including TNBC. Full article
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