Ovarialkarzinom

Bois, Andreas du; Schmalfeldt, Barbara; Meier, W.; Sehouli, Jalid; Pfisterer, Jacobus; Ovarialkarzin, die Ago Studiengruppe

doi:10.1007/s00129-006-1822-5

Cited by 1 publication

(1 citation statement)

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“…GnRH receptor is expressed in 50-64% of all human breast cancers [29][30][31][32][33] . Around 15% of all human breast cancers are stated as TNBC, which is associated with high risk recurrence and metastasis 34,35 . Approximately 74% of all TNBC express GnRH receptor 13,36,37 .…”

Section: Ctgf Differentially Regulates Potential Drivers Of Invasion mentioning

confidence: 99%

Identification of drivers of breast cancer invasion by secretome analysis: insight into CTGF signaling

Hellinger

Schömel

Buse

et al. 2020

Sci Rep

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An altered consistency of tumor microenvironment facilitates the progression of the tumor towards metastasis. Here we combine data from secretome and proteome analysis using mass spectrometry with microarray data from mesenchymal transformed breast cancer cells (MCF-7-EMT) to elucidate the drivers of epithelial-mesenchymal transition (EMT) and cell invasion. Suppression of connective tissue growth factor (CTGF) reduced invasion in 2D and 3D invasion assays and expression of transforming growth factor-beta-induced protein ig-h3 (TGFBI), Zinc finger E-box-binding homeobox 1 (ZEB1) and lysyl oxidase (LOX), while the adhesion of cell-extracellular matrix (ECM) in mesenchymal transformed breast cancer cells is increased. In contrast, an enhanced expression of CTGF leads to an increased 3D invasion, expression of fibronectin 1 (FN1), secreted protein acidic and cysteine rich (SPARC) and CD44 and a reduced cell ECM adhesion. Gonadotropin-releasing hormone (GnRH) agonist Triptorelin reduces CTGF expression in a Ras homolog family member A (RhoA)-dependent manner. Our results suggest that CTGF drives breast cancer cell invasion in vitro and therefore could be an attractive therapeutic target for drug development to prevent the spread of breast cancer.

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