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Open AccessArticle

Inhibition on JNK Mimics Silencing of Wnt-11 Mediated Cellular Response in Androgen-Independent Prostate Cancer Cells

1
Gebze Technical University, Institute of Biotechnology, 41400 Gebze-Kocaeli, Turkey
2
Istanbul Kultur University, Department of Molecular Biology and Genetics, Atakoy Campus, 34156 Istanbul, Turkey
3
School of Life Sciences, University of Bedfordshire, Park Square, Luton LU1 3JU, UK
4
Cancer Research Group, School of Life Sciences, College of Liberal Arts and Sciences, University of Westminster, 115 New Cavendish Street, London W1W 6UW, UK
*
Author to whom correspondence should be addressed.
Biology 2020, 9(7), 142; https://doi.org/10.3390/biology9070142
Received: 20 April 2020 / Revised: 10 June 2020 / Accepted: 25 June 2020 / Published: 27 June 2020
Prostate cancer (PCa) is one of the most common cancers among men, and one of the leading causes of cancer death for men. The c-Jun N-terminal kinase (JNK) pathway is required for several cellular functions, such as survival, proliferation, differentiation, and migration. Wnt-11, a member of the Wnt family, has been identified for its upregulation in PCa; however, downstream signalling of Wnt-11 remains to be fully characterized. In this study, we investigated the role of the JNK pathway as a potential downstream factor for Wnt-11 signalling. For this purpose, LNCaP, DU145, and PC-3 PCa cells and normal epithelial PNT1A cells were treated with a specific JNK kinase inhibitor: JNKVIII. Our results showed that JNK inhibition decreased mitochondrial membrane potential and promoted cell death in a cell type-dependent manner. We found that JNK inhibition led to an increase in autophagy and prevented epithelial–mesenchymal transition (EMT) in independently growing androgen cells. JNK inhibition and the silencing of Wnt-11 showed similar responses in DU145 and PC-3 cells and decreased metastasis-related biomarkers, cell migration, and invasion. Overall, our results suggest that JNK signalling plays a significant role in the pathophysiology of PCa by mediating Wnt-11 induced signals. Our data highlights that both the JNK pathway and Wnt-11 could be a useful therapeutic target for the combinatory application of current PCa. View Full-Text
Keywords: c-Jun signalling; prostate cancer; apoptosis; Wnt-11; neuroendocrine-like differentiation c-Jun signalling; prostate cancer; apoptosis; Wnt-11; neuroendocrine-like differentiation
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Arisan, E.D.; Rencuzogullari, O.; Keskin, B.; Grant, G.H.; Uysal-Onganer, P. Inhibition on JNK Mimics Silencing of Wnt-11 Mediated Cellular Response in Androgen-Independent Prostate Cancer Cells. Biology 2020, 9, 142.

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