Ganglioside composition correlates with the malignant phenotype of cholangiocarcinoma cells and modulates cell adhesion

AbstractWe recently reported that human melanoma cells, but not benign melanocytes, aberrantly express kallikrein-related peptidase 7 (KLK7). Here, we show a KLK7 overexpression-mediated decrease of cell adhesion to extracellular matrix binding proteins, associated with downregulation of α5/β1/αv/β3 integrin expression. We also report an up-regulation of MCAM/CD146 and an increase in spheroid formation of these cells. Our results demonstrate that aberrant KLK7 expression leads to a switch to a more malignant phenotype suggesting a potential role of KLK7 in melanoma invasion. Thus, KLK7 may represent a biomarker for melanoma progression and may be a potential therapeutic target for melanoma.

Download Full-text

Glycodelin in reproductive endocrinology and hormone-related cancer

Acta Endocrinologica ◽

10.1530/eje-08-0756 ◽

2009 ◽

Vol 160 (2) ◽

pp. 121-133 ◽

Cited By ~ 39

Author(s):

M Seppälä ◽

H Koistinen ◽

R Koistinen ◽

L Hautala ◽

P C Chiu ◽

...

Keyword(s):

Cell Adhesion ◽

Immune Cells ◽

Acrosome Reaction ◽

Growth Restriction ◽

Tumour Suppressor Genes ◽

Malignant Cells ◽

Malignant Phenotype ◽

Suppressor Genes ◽

Biological Actions

Glycodelin is an endocrine-regulated glycoprotein that has significant effects on immune cells, apoptosis, reproduction, cell adhesion, differentiation and cancer. In reproduction, glycodelin contributes to capacitation and immunoprotection of spermatozoa, and it modulates sperm–oocyte binding, acrosome reaction and implantation. In endocrine-related cancer, the differentiation inducing effects of glycodelin are accompanied by growth restriction of malignant cells, decreased expression of oncogenes, increased expression of tumour suppressor genes and morphological reversion of the malignant phenotype. This review features these properties and clinical connections, highlighting the role of glycosylation in biological actions.

Download Full-text

The tale of a tail: The secret behind IGF-1R’s oncogenic power

Science Signaling ◽

10.1126/scisignal.abb7887 ◽

2020 ◽

Vol 13 (633) ◽

pp. eabb7887

Author(s):

Caitrin Crudden ◽

Leonard Girnita

Keyword(s):

Plasma Membrane ◽

Cell Adhesion ◽

Growth Factor ◽

Dependent Manner ◽

Insulin Like Growth Factor ◽

Malignant Phenotype ◽

A Cell ◽

Migratory Cells

The C-terminal tail of insulin-like growth factor 1 receptor (IGF-1R) has long been appreciated to drive much of this receptor’s oncogenic power. In this issue of Science Signaling, Rieger et al. have shown that Tyr1250 and Tyr1251 of IGF-1R are autophosphorylated in a cell adhesion–dependent manner, uncovering a previously unknown plasma membrane–Golgi trafficking route for IGF-1R in migratory cells, an integral part of the malignant phenotype.

Download Full-text