Sina Grebhardt

Learn More
S100A8 and S100A9, two heterodimer-forming members of the cytosolic S100 Ca(2+) signaling protein family, are overexpressed in various cancer types, including prostate cancer. They act as proinflammatory danger signals when secreted to the extracellular space and are thought to play an important role during tumorigenesis, affecting inflammatory processes,(More)
FOLFOX is a cytostatic drug combination for adjuvant treatment of colorectal cancer (CRC) consisting of 5-fluorouracil (5-FU), leucovorin, and oxaliplatin. The mechanism of synergistic interaction of these drugs is poorly understood and little is known concerning the role of drug transporters and the impact of oxaliplatin metabolites oxalate and(More)
Estrogen receptor α (ERα) functions as a transcription factor to regulate a wide range of cellular activities in response to 17β-estradiol (E2). The regulation of ERα transcriptional activity is highly complex and not yet fully understood. In this respect, recent studies have highlighted the importance of certain cellular protein kinases. To identify novel(More)
The proinflammatory S100A8/A9 proteins, which are expressed in myeloid cells under physiological conditions, are strongly expressed in human prostate cancer epithelial cells. Their role in the tumor cells and in tumor progression is largely unclear. We established a prostate cancer epithelial cell line (PC-3 TO-A8/A9) expressing S100A8 and S100A9(More)
Estrogen receptor-alpha (ERα) is a key factor in the development of breast cancer in humans. The expression and activity of ERα is regulated by a multitude of intracellular and extracellular signals. Here we show a cross-talk between β-catenin and ERα in human breast cancer cells. Knockdown of β-catenin by RNAi resulted in significant reduction of ERα mRNA(More)
S100A8 and S100A9 are strongly expressed in epithelial cells of human prostate cancer. However, the regulation of their expression is unclear. Here we show that S100A8 and to a lesser extent S100A9 mRNA expression is induced by prostaglandin E2 in a dose and time-dependent manner in PC-3 prostate cancer cells as well as in BPH-1 benign prostatic epithelial(More)
  • 1