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Volume 3, Issue 6, pp. 165 - 207, June 2019

Issue cover
Cover: This month in Cell Stress: Mitochondria-related hallmarks of reprogramming. Image depicts a fibroblast (elongated mitochondrial network) that has been reprogrammed into an induced pluripotent stem cell (fragmented mitochondrial network). The image highlights mitochondrial morphology changes during cellular reprogramming. Image conceptualized by Megan Rasmussen and designed by Ella Marushchenko and Alexander Tokarev (Ella Maru Studio, Inc.). The cover is published under the CC BY 4.0 license. Enlarge issue cover


Biology and clinical relevance of EpCAM

Laura Keller, Stefan Werner and Klaus Pantel

page 165-180 | 10.15698/cst2019.06.188 | Full text | PDF | Abstract

Epithelial cell adhesion molecule (EpCAM) is a transmembrane glycoprotein primarily known to mediate homotypic cell contacts in epithelia tissues. Because EpCAM expression is limited to normal and malignant epithelia, it has been used as diagnostic marker for the detection of carcinoma cells in mesenchymal organs such as blood, bone marrow or lymph nodes. In particular, the detection and molecular characterization of EpCAM-positive circulating tumor cells (CTCs) in the blood of carcinoma patients has gained considerable interest over the past ten years. EpCAM is primarily considered as an adhesion molecule, but recent studies have shown diverse biological functions including regulation of cell proliferation and cancer stemness. In this review, we summarize the current knowledge on the biological properties of EpCAM with emphasis on mechanisms involved in cancer progression and discuss the clinical implications of these findings for the clinical use of EpCAM as a diagnostic marker.

Remodeling of mitochondrial morphology and function: an emerging hallmark of cellular reprogramming

Anuj Rastogi, Piyush Joshi, Ela Contreras and Vivian Gama

page 181-194 | 10.15698/cst2019.06.189 | Full text | PDF | Abstract

Research in the stem cell field has traditionally focused on understanding key transcriptional factors that provide pluripotent cell identity. However, much less is known about other critical non-transcriptional signaling networks that govern stem cell identity. Although we continue to gain critical insights into the mechanisms underlying mitochondrial morphology and function during cellular reprogramming – the process of reverting the fate of a differentiated cell into a stem cell, many uncertainties remain. Recent studies suggest an emerging landscape in which mitochondrial morphology and function have an active role in maintaining and regulating changes in cell identity. In this review, we will focus on these emerging concepts as crucial modulators of cellular reprogramming. Recognition of the widespread applicability of these concepts will increase our understanding of the mitochondrial mechanisms involved in cell identity, cell fate and disease.

The sensing of mitochondrial DAMPs by non-immune cells

Aida Rodríguez-Nuevo and Antonio Zorzano

page 195-207 | 10.15698/cst2019.06.190 | Full text | PDF | Abstract

Mitochondria are the source of damage-associated molecular patterns (DAMPs), which are molecules that play a key modulatory role in immune cells. These molecules include proteins and peptides, such as N-formyl peptides and TFAM, as well as lipids, and metabolites such as cardiolipin, succinate and ATP, and also mitochondrial DNA (mtDNA). Recent data indicate that somatic cells sense mitochondrial DAMPs and trigger protective mechanisms in response to these signals. In this review we focus on the well-described effects of mitochondrial DAMPs on immune cells and also how these molecules induce immunogenic responses in non-immune cells. Special attention will be paid to the response to mtDNA.

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