Jana Samarin
University Hospital Heidelberg
6 Papers
Jana Samarin is an academic researcher from University Hospital Heidelberg. The author has contributed to research in topics: Internal medicine & Ubiquitin ligase. The author has an hindex of 5, co-authored 5 publications. Previous affiliations of Jana Samarin include Heidelberg University.
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Papers
Autocrine insulin‐like growth factor‐II stimulation of tumor cell migration is a progression step in human hepatocarcinogenesis
Tanja Nussbaum,Jana Samarin,Volker Ehemann,Michaela Bissinger,Eduard Ryschich,Akmal Khamidjanov,Xiaolei Yu,Norbert Gretz,Peter Schirmacher,Kai Breuhahn +9 more
TL;DR: Activation of IGF‐II/IGF‐IR signaling is likely a progression switch selected by function that promotes tumor cell dissemination and aggressive tumor behavior.
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Nuclear expression of the ubiquitin ligase seven in absentia homolog (SIAH)-1 induces proliferation and migration of liver cancer cells
A Brauckhoff,Mona Malz,Darjus F. Tschaharganeh,Nisar P. Malek,Achim Weber,Marc-Oliver Riener,Christopher Soll,Jana Samarin,Michaela Bissinger,Jan Schmidt,Thomas Longerich,Volker Ehemann,Peter Schirmacher,Kai Breuhahn +13 more
TL;DR: Interference with SIAH-1 activity represents a promising approach to suppress HCC growth and supports different pro-tumorigenic cellular processes associated with tumor growth and tumor cell dissemination in human hepatocarcinogenesis.
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Nuclear accumulation of seven in absentia homologue-2 supports motility and proliferation of liver cancer cells
Mona Malz,Antje Aulmann,Jana Samarin,Michaela Bissinger,Thomas Longerich,Sabrina Schmitt,Peter Schirmacher,Kai Breuhahn +7 more
TL;DR: Data show that SIAH‐2—as described for SIAh‐1—accumulates in nuclei of HCC cells where it supports tumor growth and tumor cell dissemination, and represents a promising therapeutic strategy for HCC.
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Overexpression of far upstream element (FUSE) binding protein (FBP)‐interacting repressor (FIR) supports growth of hepatocellular carcinoma
Mona Malz,Michael Bovet,Jana Samarin,Uta Rabenhorst,Carsten Sticht,Michaela Bissinger,Stephanie Roessler,Justo Lorenzo Bermejo,Marcus Renner,Diego F. Calvisi,Stephan Singer,Matthias Ganzinger,Achim Weber,Norbert Gretz,Martin Zörnig,Peter Schirmacher,Kai Breuhahn +16 more
TL;DR: High‐level nuclear FIR does not facilitate repressor properties but supports tumor growth in HCC cells, suggesting that the pharmacological inhibition of FIR might represent a promising therapeutic strategy for HCC patients with elevated FIR expression.
Low level of antioxidant capacity biomarkers but not target overexpression predicts vulnerability to ROS-inducing drugs
Jana Samarin,Piotr Fabrowski,Roman Vladimirovich Kurilov,Hana Nůsková,Johanna Hummel-Eisenbeiss,Hannelore Pink,Nan Li,V. Weru,Hamed Alborzinia,Umut Yildiz,Laura Grob,Minerva Taubert,Marie C Czech,Michael Morgen,Christina Brandstädter,Katja Becker,Lianghao Mao,Ashok Kumar Jayavelu,Angela Goncalves,Ulrike Uhrig,Jeanette Seiler,Yanhong Lyu,Sven Diederichs,Ursula Klingmüller,Martina U. Muckenthaler,Annette Kopp-Schneider,Aurelio A. Teleman,Aubry K. Miller,Nikolas Gunkel +28 more
TL;DR: In this paper , a set of "antioxidant-capacity" biomarkers (ACB) were identified, which were tightly repressed, partly by STAT3 and STAT5A/B in sensitive cells, rendering them susceptible to multiple redox-targeting and ferroptosis-inducing drugs.