A5091824396- Cancer Cells and Metastasis
- Cancer Research and Treatments
- Mesenchymal stem cell research
- Immunotherapy and Immune Responses
- Cell Adhesion Molecules Research
- HER2/EGFR in Cancer Research
- Cancer Genomics and Diagnostics
- Chemokine receptors and signaling
- Virus-based gene therapy research
- Microtubule and mitosis dynamics
- Biomedical Ethics and Regulation
- Cancer-related Molecular Pathways
- Hematopoietic Stem Cell Transplantation
- Advanced oxidation water treatment
- Pluripotent Stem Cells Research
- Corporate Governance and Management
- Tissue Engineering and Regenerative Medicine
- CAR-T cell therapy research
- Water Treatment and Disinfection
- Epigenetics and DNA Methylation
- Periodontal Regeneration and Treatments
- Cancer, Hypoxia, and Metabolism
- 3D Printing in Biomedical Research
- Fluorine in Organic Chemistry
- Angiogenesis and VEGF in Cancer
Witten/Herdecke University
2015-2024
TU Dresden
2008-2022
Institute of Immunology
2006-2014
Eppendorf (Germany)
2008
Software (Spain)
2008
University of California, Berkeley
2007
University Hospital Münster
2007
Marien Hospital Witten
2004
Friedrich Schiller University Jena
2003-2004
Augsburg University
1999
Induction of tumor cell migration is a key step in invasion and metastasis. Here we report that the epidermal growth factor (EGF)-induced breast cancer cells attributed to transient, rather than sustained, activation phospholipase C (PLC)-gamma1 due c-erbB-2 signaling. EGF stimulation receptor (EGFR) overexpressing resulted long-term PLC-gamma1 tyrosine phosphorylation sustained levels inositol-1,4,5-triphosphate (IP3) diacylglycerol (DAG) producing sinusoidal calcium oscillations. In...
HER2 signalling by heterodimerisation with EGFR and HER3 in breast cancer is associated worst outcome of the afflicted patients, which attributed not only to aggressiveness such tumours but also therapy resistance. Thus, present study we investigated role EGFR, lateral cell migration applying MDA-MB-468-HER2 (MDA-HER2) line, representing a valid model system. Knockdown expression siRNA resulted decreased phosphorylated AKT (pAKT) levels, abrogated epidermal growth factor (EGF)-mediated...
Separate mechanisms for oncogenesis and metastasis have been postulated. We show here that prolonged invasive cell migration, a key mechanism in cancer metastasis, is linked to c-erbB-2 signaling. Cell lines with EGFR expression transphosphorylation activity display high transendothelial invasiveness an endothelial-extra-cellular matrix model mimicking capillary vessel wall vitro. Tyrosine-phosphorylated receptors are localized predominantly areas of the membrane extension activity. On...
In addition to physiological events such as fertilisation, placentation, osteoclastogenesis, or tissue regeneration/wound healing, cell fusion is involved in pathophysiological conditions cancer. Cell fusion, which applies both the proteins and that induce merging of two more cells, not a fully understood process. Inflammation/pro-inflammatory cytokines might be positive trigger for fusion. Using Cre-LoxP-based assay we demonstrated between human M13SV1-Cre breast epithelial cells...
Monocytes originate from precursors made in the bone and remain circulation for nearly 24 h. Much effort has been done to identify molecules regulating transendothelial migration of monocytes during inflammatory conditions. In contrast, considerably less is known about process constitutive monocyte emigration although 340 million leave each day healthy individuals. Previous studies indicated that chemokines were up-regulated cocultured with endothelial cells induce retraction latter cell...
The biological phenomenon of cell fusion has been associated with cancer progression since it was determined that normal × tumor fusion-derived hybrid cells could exhibit novel properties, such as enhanced metastatogenic capacity or increased drug resistance, and even a mechanism give rise to stem/initiating (CS/ICs). CS/ICs have proposed stem including the ability (re)initiate growth.
To date, several studies have confirmed that driving forces of the inflammatory tumour microenvironment trigger spontaneous cancer cell fusion. However, less is known about underlying factors and mechanisms facilitate inflammation-induced fusion a with normal cell. Recently, we demonstrated minocycline, tetracycline antibiotic, successfully inhibited TNF-α-induced MDA-MB-435 cells M13SV1 breast epithelial cells. Here, investigated how minocycline interferes TNF-α induced signal transduction...