CEACAM6 x CD3 x CEACAM5

Last update 01 Nov 2024

Basic Info

Related Targets

CEACAM6CD3CEACAM5

Drugs associated with CEACAM6 x CD3 x CEACAM5

PM-4008

Target

CD3 x CEACAM5 x CEACAM6

Mechanism

CD3 inhibitors [+2]

Active Org.-

Originator Org.

Pumis Biotechnology (Zhuhai) Co., Ltd.Startup

Active Indication-

Inactive Indication

Neoplasms

Drug Highest PhaseDiscontinued

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with CEACAM6 x CD3 x CEACAM5

100 Translational Medicine associated with CEACAM6 x CD3 x CEACAM5

0 Patents (Medical) associated with CEACAM6 x CD3 x CEACAM5

Literatures (Medical) associated with CEACAM6 x CD3 x CEACAM5

PLoS ONEQ3 · CROSS-FIELD

Tumor and Endothelial Cell-Derived Microvesicles Carry Distinct CEACAMs and Influence T-Cell Behavior

Q3 · CROSS-FIELD

ArticleOA

Author: Janine D. Dreesen ; Harrison T. Muturi ; Bernhard B. Singer ; Bernd Giebel ; Holger Jastrow ; Suleyman Ergun ; Elena Nilewski

Normal and malignant cells release a variety of different vesicles into their extracellular environment. The most prominent vesicles are the microvesicles (MVs, 100-1000 nm in diameter), which are shed of the plasma membrane, and the exosomes (70-120 nm in diameter), derivates of the endosomal system. MVs have been associated with intercellular communication processes and transport numerous proteins, lipids and RNAs. As essential component of immune-escape mechanisms tumor-derived MVs suppress immune responses. Additionally, tumor-derived MVs have been found to promote metastasis, tumor-stroma interactions and angiogenesis. Since members of the carcinoembryonic antigen related cell adhesion molecule (CEACAM)-family have been associated with similar processes, we studied the distribution and function of CEACAMs in MV fractions of different human epithelial tumor cells and of human and murine endothelial cells. Here we demonstrate that in association to their cell surface phenotype, MVs released from different human epithelial tumor cells contain CEACAM1, CEACAM5 and CEACAM6, while human and murine endothelial cells were positive for CEACAM1 only. Furthermore, MVs derived from CEACAM1 transfected CHO cells carried CEACAM1. In terms of their secretion kinetics, we show that MVs are permanently released in low doses, which are extensively increased upon cellular starvation stress. Although CEACAM1 did not transmit signals into MVs it served as ligand for CEACAM expressing cell types. We gained evidence that CEACAM1-positive MVs significantly increase the CD3 and CD3/CD28-induced T-cell proliferation. All together, our data demonstrate that MV-bound forms of CEACAMs play important roles in intercellular communication processes, which can modulate immune response, tumor progression, metastasis and angiogenesis.

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