EMT and MET as paradigms for cell fate switching

Chen, Jiekai; Han, Qingkai; Pei, Duanqing

doi:10.1093/jmcb/mjr045

Cited by 47 publications

(40 citation statements)

References 19 publications

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“…The epithelial cells that line the surface of a tissue or organ are attached to the basement membrane, establishing an apical-basal axis of polarity, and communicating with each other through the gap junction, generally not exhibiting a regimented structure or tight intracellular adhesion (12,13). Mesenchymal cells form structures that are irregular in shape and not uniform in composition or density.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-146a inhibits epithelial mesenchymal transition in non-small cell lung cancer by targeting insulin receptor substrate 2

Park

Jeon

Lee

et al. 2015

International Journal of Oncology

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Abstract. During cancer progression, some tumor cells show changes in their plasticity by morphological and phenotypical conversions, as an expression of mesenchymal markers and loss of epithelial markers, collectively referred to as epithelialmesenchymal transition (EMT). EMT has been increasingly recognized as a critical phenomenon in lung cancer progression. The goal of this study was to identify microRNAs involved in lung cancer progression. A microarray and qRT-PCR were performed to investigate the miRNA expression profiles in mesenchymal-like lung cancer cells. The role of miR-146a in lung cancer progression was measured by invasion and migration assays in vitro. Bioinformatics and luciferase report assays were used to identify the target of miR-146a. The expression of miR-146a was reduced in mesenchymal-like lung cancer cell lines. The overexpression of miR-146a induced a marked reduction of the mesenchymal marker and increase the epithelial marker in lung cancer cell lines. Moreover, the overexpression of miR-146a suppressed lung cancer cell migration and invasion. Co-treatment with miR-146a and gefitinib treatment showed a significant reduction of invasion in the resistant lung cancer cells induced by EMT. The expression of miR-146a was downregulated in advanced lung cancer tissues. Insulin receptor substrate 2 (IRS2), an adaptor protein that modulates normal growth, metabolism, survival, and differentiation, was identified as a target of miR-146a. miR-146a regulated the expression of IRS2 at the mRNA and protein levels. These data demonstrate for the first time that miR-146a suppresses lung cancer progression by repressing IRS2 expression. This provides new insight into the post-transcriptional regulation of lung cancer progression by miRNAs, a potential approach for the treatment of lung cancer.

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Section: Discussionmentioning

confidence: 99%

MicroRNA-146a inhibits epithelial mesenchymal transition in non-small cell lung cancer by targeting insulin receptor substrate 2

Park

Jeon

Lee

et al. 2015

International Journal of Oncology

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“…2). The primitive streak constitutes a gate through which cells migrate from the epiblast into the interior of the embryo via an epithelial-tomesenchymal transition (EMT) (Thiery et al, 2009;Chen et al, 2012). Therefore, the morphological process of EMT is coupled with the first cell fate decision -the generation of three germ layersof the embryo.…”

Section: Several Routes To Pluripotency: Mechanisms Of Cell Reprogrammentioning

confidence: 99%

A developmental framework for induced pluripotency

2015

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During development, cells transition from a pluripotent to a differentiated state, generating all the different types of cells in the body. Development is generally considered an irreversible process, meaning that a differentiated cell is thought to be unable to return to the pluripotent state. However, it is now possible to reprogram mature cells to pluripotency. It is generally thought that reprogramming is accomplished by reversing the natural developmental differentiation process, suggesting that the two mechanisms are closely related. Therefore, a detailed study of cell reprogramming has the potential to shed light on unexplained developmental mechanisms and, conversely, a better understanding of developmental differentiation can help improve cell reprogramming. However, fundamental differences between reprogramming processes and multi-lineage specification during early embryonic development have also been uncovered. In addition, there are multiple routes by which differentiated cells can re-enter the pluripotent state. In this Review, we discuss the connections and disparities between differentiation and reprogramming, and assess the degree to which reprogramming can be considered as a simple reversal of development.

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“…Hence the emergence npg of M-Grand and E-Grand divisions is also associated with the appearance of cadherins and the acquisition of an epithelium in evolution. This evolutionary paradigm also mirrors the acquisition of E-cadherin in a developing mammalian embryo: a loose collection of essentially identical single cells (blastomeres) form an epithelial sheet (compaction of the morula) with the expression of E-cadherin which then undergo gastrulation to acquire specialized organs and tissues during which EMT/MET events appear to dominate [9].…”

mentioning

confidence: 90%