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1. Road to Metastasis: The TWEAK Pathway as a Discriminant between Metastasizing and Non-Metastasizing Thick Melanomas

Author

Canan Güvenç, Asier Antoranz, Anna Szumera-Ciećkiewicz, Pawel P. Teterycz, Piotr R. Rutkowski, Robert V. Rawson, Richard A. Scolyer, John F. Thompson, Julia Newton-Bishop, Marguerite Stas, Veerle Boecxstaens, Oliver Bechter, Jurgen Vercauteren, Marjan Garmyn, Joost van den Oord, and Francesca Maria Bosisio

Subjects
melanoma, thick Breslow, TWEAK pathway, Biology (General), QH301-705.5, Chemistry, QD1-999
Abstract

Cutaneous melanoma (CM) is the most aggressive form of skin cancer, and its worldwide incidence is rapidly increasing. Early stages can be successfully treated by surgery, but once metastasis has occurred, the prognosis is poor. However, some 5–10% of thick (≥2 mm) melanomas do not follow this scenario and run an unpredictable course. Little is known about the factors that contribute to metastasis in some patient with thick melanomas and the lack thereof in thick melanoma patients who never develop metastatic disease. We were therefore interested to study differential gene expression and pathway analysis and compare non-metastatic and metastatic thick melanomas. We found that the TNF-like weak inducer of apoptosis (TWEAK) pathway was upregulated in thick non-metastasizing melanomas. MAP3K14 (NIK1), BIRC2 (cIAP1), RIPK1, CASP7, CASP8, and TNF play an important role in inhibiting proliferation and invasion of tumor cells via the activation of the non-canonical NF-κB signaling pathway. In particular, this pathway sensitizes melanoma cells to TNF-alpha and activates the apoptosis module of the TWEAK pathway in thick non-metastasizing melanomas. Hence, our study suggests a potential role of the TWEAK pathway in inhibiting thick melanoma from metastasis. Exploitation of these genes and the pathway they control may open future therapeutic avenues.

Published
2021
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2. Road to Metastasis: The TWEAK Pathway as a Discriminant between Metastasizing and Non-Metastasizing Thick Melanomas

Author

Robert V. Rawson, Asier Antoranz, Anna Szumera-Ciećkiewicz, Richard A. Scolyer, Jurgen Vercauteren, Paweł Teterycz, John F. Thompson, Marjan Garmyn, Marguerite Stas, Joost van den Oord, Piotr R. Rutkowski, Veerle Boecxstaens, Francesca Maria Bosisio, Oliver Bechter, Canan Güvenç, and Julia Newton-Bishop

Subjects
Male, Skin Neoplasms, CUTANEOUS MELANOMA, Chemistry, Multidisciplinary, TWEAK pathway, ANGIOGENESIS, Metastasis, Cohort Studies, RNA-Seq, Biology (General), Neoplasm Metastasis, Spectroscopy, Melanoma, Communication, PROLIFERATION, Cytokine TWEAK, General Medicine, Middle Aged, Prognosis, CANCER, Computer Science Applications, thick Breslow, APOPTOSIS, Gene Expression Regulation, Neoplastic, Chemistry, Physical Sciences, SURVIVAL, Tumor necrosis factor alpha, Female, Signal transduction, Life Sciences & Biomedicine, Signal Transduction, Adult, Biochemistry & Molecular Biology, QH301-705.5, FUNCTIONAL EXPRESSION, Catalysis, Inorganic Chemistry, RIPK1, medicine, melanoma, Humans, Physical and Theoretical Chemistry, QD1-999, Molecular Biology, Science & Technology, COMPLEX, business.industry, Gene Expression Profiling, Organic Chemistry, medicine.disease, Apoptosis, Cutaneous melanoma, CELLS, Cancer research, OVEREXPRESSION, Skin cancer, business
Abstract

Cutaneous melanoma (CM) is the most aggressive form of skin cancer, and its worldwide incidence is rapidly increasing. Early stages can be successfully treated by surgery, but once metastasis has occurred, the prognosis is poor. However, some 5-10% of thick (≥2 mm) melanomas do not follow this scenario and run an unpredictable course. Little is known about the factors that contribute to metastasis in some patient with thick melanomas and the lack thereof in thick melanoma patients who never develop metastatic disease. We were therefore interested to study differential gene expression and pathway analysis and compare non-metastatic and metastatic thick melanomas. We found that the TNF-like weak inducer of apoptosis (TWEAK) pathway was upregulated in thick non-metastasizing melanomas. MAP3K14 (NIK1), BIRC2 (cIAP1), RIPK1, CASP7, CASP8, and TNF play an important role in inhibiting proliferation and invasion of tumor cells via the activation of the non-canonical NF-κB signaling pathway. In particular, this pathway sensitizes melanoma cells to TNF-alpha and activates the apoptosis module of the TWEAK pathway in thick non-metastasizing melanomas. Hence, our study suggests a potential role of the TWEAK pathway in inhibiting thick melanoma from metastasis. Exploitation of these genes and the pathway they control may open future therapeutic avenues. ispartof: INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES vol:22 issue:19 ispartof: location:Switzerland status: published

Published
2021

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