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Your search keyword '"Mathas S"' showing total 2 results
Start Over Author "Mathas S" Journal molecular cancer
2 results on '"Mathas S"'

1. PDGFRβ promotes oncogenic progression via STAT3/STAT5 hyperactivation in anaplastic large cell lymphoma

Author

Garces de los Fayos Alonso, I., Zujo, L., Wiest, I., Kodajova, P., Timelthaler, G., Edtmayer, S., Zrimšek, M., Kollmann, S., Giordano, C., Kothmayer, M., Neubauer, H. A., Dey, S., Schlederer, M., Schmalzbauer, B. S., Limberger, T., Probst, C., Pusch, O., Högler, S., Tangermann, S., Merkel, O., Schiefer, A. I., Kornauth, C., Prutsch, N., Zimmerman, M., Abraham, B., Anagnostopoulos, J., Quintanilla-Martinez, L., Mathas, S., Wolf, P., Stoiber, D., Staber, P. B., Egger, G., Klapper, W., Woessmann, W., Look, T. A., Gunning, P., Turner, S. D., Moriggl, R., Lagger, S., and Kenner, L.

Published
2022
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2. JUN mediates the senescence associated secretory phenotype and immune cell recruitment to prevent prostate cancer progression.

Author

Redmer T, Raigel M, Sternberg C, Ziegler R, Probst C, Lindner D, Aufinger A, Limberger T, Trachtova K, Kodajova P, Högler S, Schlederer M, Stoiber S, Oberhuber M, Bolis M, Neubauer HA, Miranda S, Tomberger M, Harbusch NS, Garces de Los Fayos Alonso I, Sternberg F, Moriggl R, Theurillat JP, Tichy B, Bystry V, Persson JL, Mathas S, Aberger F, Strobl B, Pospisilova S, Merkel O, Egger G, Lagger S, and Kenner L

Subjects
Male, Animals, Mice, Humans, Senescence-Associated Secretory Phenotype, Proto-Oncogene Proteins c-jun metabolism, Gene Expression Regulation, Neoplastic, Cell Line, Tumor, Gene Expression Profiling, Cellular Senescence genetics, Disease Models, Animal, Prostatic Neoplasms pathology, Prostatic Neoplasms genetics, Prostatic Neoplasms metabolism, PTEN Phosphohydrolase genetics, PTEN Phosphohydrolase metabolism, Disease Progression, Tumor Microenvironment immunology
Abstract

Background: Prostate cancer develops through malignant transformation of the prostate epithelium in a stepwise, mutation-driven process. Although activator protein-1 transcription factors such as JUN have been implicated as potential oncogenic drivers, the molecular programs contributing to prostate cancer progression are not fully understood., Methods: We analyzed JUN expression in clinical prostate cancer samples across different stages and investigated its functional role in a Pten-deficient mouse model. We performed histopathological examinations, transcriptomic analyses and explored the senescence-associated secretory phenotype in the tumor microenvironment., Results: Elevated JUN levels characterized early-stage prostate cancer and predicted improved survival in human and murine samples. Immune-phenotyping of Pten-deficient prostates revealed high accumulation of tumor-infiltrating leukocytes, particularly innate immune cells, neutrophils and macrophages as well as high levels of STAT3 activation and IL-1β production. Jun depletion in a Pten-deficient background prevented immune cell attraction which was accompanied by significant reduction of active STAT3 and IL-1β and accelerated prostate tumor growth. Comparative transcriptome profiling of prostate epithelial cells revealed a senescence-associated gene signature, upregulation of pro-inflammatory processes involved in immune cell attraction and of chemokines such as IL-1β, TNF-α, CCL3 and CCL8 in Pten-deficient prostates. Strikingly, JUN depletion reversed both the senescence-associated secretory phenotype and senescence-associated immune cell infiltration but had no impact on cell cycle arrest. As a result, JUN depletion in Pten-deficient prostates interfered with the senescence-associated immune clearance and accelerated tumor growth., Conclusions: Our results suggest that JUN acts as tumor-suppressor and decelerates the progression of prostate cancer by transcriptional regulation of senescence- and inflammation-associated genes. This study opens avenues for novel treatment strategies that could impede disease progression and improve patient outcomes., (© 2024. The Author(s).)

Published
2024
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