PIAS1 is not suitable as a urothelial carcinoma biomarker protein and pharmacological target

Autoři: Holger Hans Hermann Erb aff001;  Marlies Ebert aff001;  Ronja Kuhn aff001;  Lukas Donix aff002;  Axel Haferkamp aff001;  Robert Ian Seed aff004;  Eva Jüngel aff001
Působiště autorů: Department of Urology and Pediatric Urology, University Medical Center Mainz, Mainz, Germany aff001;  Department of Urology, Technische Universität Dresden, Dresden, Germany aff002;  National Center for Tumor Diseases (NCT), Partner Site Dresden, Germany: German Cancer Research Center (DKFZ), Heidelberg, Germany; Faculty of Medicine and University Hospital Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany and Helmhol aff003;  Department of Pathology, University of California, San Francisco, California, United States of America aff004
Vyšlo v časopise: PLoS ONE 14(10)
Kategorie: Research Article
doi: https://doi.org/10.1371/journal.pone.0224085


Urothelial cancer (UC) is one of the most common cancers in Europe and is also one of the costliest to treat. When first line therapies show initial success, around 50% of cancers relapse and proceed to metastasis. In this study we assessed the Protein inhibitor of activated signal transducers and activators of transcription (PIAS)1 as a potential therapeutic target in urothelial cancer. PIAS1 is a key regulator of STAT1 signalling and may be implicated in carcinogenesis. In contrast to other cancer types PIAS1 protein expression is not significantly different in malignant areas of UC specimens compared to non-malignant tissue. In addition, we found that down-regulation and overexpression of PIAS1 had no effect on the viability or colony forming ability of tested cell lines. Whilst other studies of PIAS1 suggest an important biological role in cancer, this study shows that PIAS1 has no influence on reducing the cytotoxic effects of Cisplatin or cell recovery after DNA damage induced by irradiation. Taken together, these in vitro data demonstrate that PIAS1 is not a promising therapeutic target in UC cancer as previously shown in different entities such as prostate cancer (PCa).

Klíčová slova:

Cancer treatment – Cell viability testing – DNA damage – DNA repair – Hyperexpression techniques – Small interfering RNAs – Transfection – SUMOylation


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