.
Cancer Metastasis
.
The
first key event in the multi-step process of metastasis is the
separation of tumor cells from the primary tumor and the dissemination
into the surrounding tissue. Cells gain the ability to migrate and
invade by altering their cytoskeletal organization, cell-cell-contacts,
contacts with the extracellular matrix (ECM) and surrounding stroma.
Epithelial-mesenchymal transition (EMT) is a transient dynamic program
induced by different transcription factors TFs). EMT-TFs orchestrate
tumor-promoting micro environmental changes, cancer cell stemness, and
chemo resistance. The contribution of EMT programs to the metastatic
cascade regarding breast cancer is supported by several publications.
However, it is still under debate if an involvement of EMT programs is
indispensable for creating an invasive phenotype. Therefore it is
necessary to study cancer cell invasion with regards to EMT complexity.
.
.
Funding:
-
Deutsche Krebshilfe, approved on 05/15/2006
for 3 years: Influence of GnRH analogs on bone-directed metastasis of breast cancer cells
in vitro and in vivo.
-
Deutsche Krebshilfe, approved on 04/17/2009
for 3 years: Effects of gene products of the metastasis-suppressor-gene KISS1 on proliferation,
metastasis and gene expression of breast cancers in vitro and in vivo.
- Deutsche Krebshilfe, approved on 09/16/2016
for 3 years: Signaling pathways of cell invasion as target for the therapy of metastatic breast cancer.
.
Publications:
-
Hellinger
JW, Hüchel S, Goetz L, Bauerschmitz G, Emons G, Gründker
C (2019) Inhibition of CYR61-S100A4 axis limits breast cancer
invasion. Frontiers in Oncology 9:1074
-
Gründker C,
Läsche M, Hellinger JW, Emons G (2019) Mechanisms of metastasis
and cell mobility: The role of metabolism. Geburtshilfe und Frauenheilkunde 79: 184-188
-
Gründker C, Emons G (2017) The Role of Gonadotropin-Releasing Hormone in Cancer Cell Proliferation and Metastasis. Frontiers in Endocrinology 8:187
-
Gründker
C, Bauerschmitz G, Schubert A, Emons G (2016) Invasion and increased
expression of S100A4 and CYR61 in mesenchymal transformed breast cancer
cells is downregulated by GnRH. International Journal of Oncology 48(6):2713-2721
-
Gründker C, Bauerschmitz G,
Knapp J, Schmidt E, Olbrich T, Emons G (2015) Inhibition of SDF-1/CXCR4
system-induced epithelial-mesenchymal transition by kisspeptin-10. Breast Cancer Reseach and Treatment 152(1):41-50
-
Ziegler E, Hansen M-T, Haase M, Emons G, Gründker C (2014) Generation of MCF-7 cells with aggressive metastatic potential in vitro and in vivo. Breast Cancer Research and Treatment 148(2):269-277
-
Schmidt E, Haase M, Ziegler E,
Emons G, Gründker C (2014) Kisspeptin-10 inhibits stromal-derived factor-1-induced
invasion of human endometrial cancer cells. International Journal of Gynecological Cancer 24(2):210-217
-
Ziegler E, Olbricht T, Emons G, Gründker
C (2013) Antiproliferative effects of kisspeptin-10 depend on
artificial GPR54 (KiSS1R) expression levels. Oncology Reports 29(2):549-554
-
Schubert A, Hawighorst
T, Emons G, Gründker C (2011) Agonist and antagonists of GnRH-I and -II reduce metastasis
of triple-negative human breast cancer cells in vivo. Breast Cancer Research
and Treatment 130(3):783-790
-
Olbrich T, Ziegler E, Türk G, Schubert A, Emons
G, Gründker C (2010) Kisspeptin-10 inhibits bone-directed migration of GPR54-positive
breast cancer cells: evidence for a dose-window effect. Gynecologic Oncology 119:571-578
-
Schubert A, Schulz
H, Emons G, Gründker C (2008) Expression of OPG and RANKL in HCC70 breast cancer cells
and effects of GnRH treatment on RANKL expression. Gynecological
Endocrinology 24(6):331-338
-
von Alten J, Fister
S, Schulz H, Viereck V, Frosch KH, Emons G, Gründker C (2006) GnRH analogs reduce
invasiveness of human breast cancer cells. Breast Cancer Research and Treatment
100:13-21
|
|
|
|
