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Alterations to Signalling Pathways in Cancer Cells 2024

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

Deadline for manuscript submissions: closed (15 March 2024) | Viewed by 1662

Special Issue Editor

Special Issue Information

Dear Colleagues,

It is well acknowledged that in most transformed and tumour cells, intracellular signalling pathways are altered to be similar to those observed in untransformed cells. Considerable interest has been focused on understanding how these signalling pathways have been altered and how these differences can be used to devise potential therapeutic treatments that may enhance survival rates of cancer patients. In the area of melanoma research, much effort has been directed to understanding how those cells containing the BRAFV600E mutation can overcome treatment with specific inhibitors such as vemurafenib. This Special Issue of the International Journal of Molecular Sciences, “Alterations to Signalling Pathways in Cancer Cells 2023” will focus on how intracellular signalling pathways are altered in tumour cells. Authors are invited to submit manuscripts that compare how these pathways differ to those seen in untransformed cells, and how they differ to those seen in untransformed cells or in tumour cells undergoing treatment. The results from these studies may provide useful information in devising treatments that may enhance the survival rates of cancer patients.

Dr. Terrence Piva
Guest Editor

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Published Papers (1 paper)

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Research

22 pages, 3878 KiB  
Article
BMP Stimulation Differentially Affects Phosphorylation and Protein Stability of β-Catenin in Breast Cancer Cell Lines
by Mustafa Ilhan, Nurcan Hastar, Branka Kampfrath, Deniz Neslihan Spierling, Jerome Jatzlau and Petra Knaus
Int. J. Mol. Sci. 2024, 25(9), 4593; https://doi.org/10.3390/ijms25094593 - 23 Apr 2024
Viewed by 1234
Abstract
Increased expression and nuclear translocation of β-CATENIN is frequently observed in breast cancer, and it correlates with poor prognosis. Current treatment strategies targeting β-CATENIN are not as efficient as desired. Therefore, detailed understanding of β-CATENIN regulation is crucial. Bone morphogenetic proteins (BMP) and [...] Read more.
Increased expression and nuclear translocation of β-CATENIN is frequently observed in breast cancer, and it correlates with poor prognosis. Current treatment strategies targeting β-CATENIN are not as efficient as desired. Therefore, detailed understanding of β-CATENIN regulation is crucial. Bone morphogenetic proteins (BMP) and Wingless/Integrated (WNT) pathway crosstalk is well-studied for many cancer types including colorectal cancer, whereas it is still poorly understood for breast cancer. Analysis of breast cancer patient data revealed that BMP2 and BMP6 were significantly downregulated in tumors. Since mutation frequency in genes enhancing β-CATENIN protein stability is relatively low in breast cancer, we aimed to investigate whether decreased BMP ligand expression could contribute to a high protein level of β-CATENIN in breast cancer cells. We demonstrated that downstream of BMP stimulation, SMAD4 is required to reduce β-CATENIN protein stability through the phosphorylation in MCF7 and T47D cells. Consequently, BMP stimulation reduces β-CATENIN levels and prevents its nuclear translocation and target gene expression in MCF7 cells. Conversely, BMP stimulation has no effect on β-CATENIN phosphorylation or stability in MDA-MB-231 and MDA-MB-468 cells. Likewise, SMAD4 modulation does not alter the response of those cells, indicating that SMAD4 alone is insufficient for BMP-induced β-CATENIN phosphorylation. While our data suggest that considering BMP activity may serve as a prognostic marker for understanding β-CATENIN accumulation risk, further investigation is needed to elucidate the differential responsiveness of breast cancer cell lines. Full article
(This article belongs to the Special Issue Alterations to Signalling Pathways in Cancer Cells 2024)
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