Author Correction: MicroRNA-146a directs the symmetric division of Snail-dominant colorectal cancer stem cells.

In the version of Supplementary Fig. 6c originally published with this Article, the immunoprecipitation (IP) and immunoblotting (IB) tags in the top panel were mislabelled. In addition, in Supplementary Fig.

HSP60 overexpression increases the protein levels of the p110α subunit of phosphoinositide 3-kinase and c-Myc.

Heat shock protein 60 (HSP60) is a chaperone protein which plays an essential role in facilitating the folding of many newly synthesized proteins to reach their native forms. Increased HSP60 expression is observed in various types of human cancers. However, proteins induced by HSP60 to mediate transformation remain largely unknown.

TET1 regulates hypoxia-induced epithelial-mesenchymal transition by acting as a co-activator.

Background: Hypoxia induces the epithelial-mesenchymal transition, EMT, to promote cancer metastasis. In addition to transcriptional regulation mediated by hypoxia-inducible factors, HIFs, other epigenetic mechanisms of gene regulation, such as histone modifications and DNA methylation, are utilized under hypoxia. However, whether DNA demethylation mediated by TET1, a DNA dioxygenase converting 5-methylcytosine, 5mC, into 5-hydroxymethylcytosine, 5hmC, plays a role in hypoxia-induced EMT is largely unknown.

MicroRNA-146a directs the symmetric division of Snail-dominant colorectal cancer stem cells.

Asymmetrical cell division (ACD) maintains the proper number of stem cells to ensure self-renewal. In cancer cells, the deregulation of ACD disrupts the homeostasis of the stem cell pool and promotes tumour growth. However, this mechanism is unclear.

Epigenetic regulation of hypoxia-responsive gene expression: focusing on chromatin and DNA modifications.

Mammalian cells constantly encounter hypoxia, which is a stress condition occurring during development and physiological processes. To adapt to this inevitable condition, cells develop various mechanisms to cope with this stress and survive. In addition to the activation/stabilization of transcriptional regulators (hypoxia-inducible factors), other epigenetic mechanisms of gene regulation are used.

Hypoxia-regulated target genes implicated in tumor metastasis.

Hypoxia is an important microenvironmental factor that induces cancer metastasis. Hypoxia/hypoxia-inducible factor-1α (HIF-1α) regulates many important steps of the metastatic processes, especially epithelial-mesenchymal transition (EMT) that is one of the crucial mechanisms to cause early stage of tumor metastasis. To have a better understanding of the mechanism of hypoxia-regulated metastasis, various hypoxia/HIF-1α-regulated target genes are categorized into different classes including transcription factors, histone modifiers, enzymes, receptors, kinases, small GTPases, transporters, adhesion molecules, surface molecules, membrane proteins, and microRNAs.

Epigenetic reprogramming and post-transcriptional regulation during the epithelial-mesenchymal transition.

The epithelial-mesenchymal transition (EMT) is a developmental process that is important for organ development, metastasis, cancer stemness, and organ fibrosis. The EMT process is regulated by different signaling pathways as well as by various epigenetic and post-transcriptional mechanisms. Here, we review recent progress describing the role of different chromatin modifiers in various signaling events leading to EMT, including hypoxia, transforming growth factor (TGF)-β, Notch, and Wnt.

Interplay between HDAC3 and WDR5 is essential for hypoxia-induced epithelial-mesenchymal transition.

Epithelial-mesenchymal transition (EMT) is important for organ development, metastasis, cancer stemness, and organ fibrosis. Molecular mechanisms to coordinately regulate hypoxia-induced EMT remain elusive. Here, we show that HIF-1α-induced histone deacetylase 3 (hdac3) is essential for hypoxia-induced EMT and metastatic phenotypes.

Interaction between HSP60 and beta-catenin promotes metastasis.

Heat shock protein 60 (HSP60) plays an essential role in assisting many newly synthesized proteins to reach their native forms. Increased HSP60 expression is observed in different types of human cancers with metastasis (e.g.

Direct regulation of HSP60 expression by c-MYC induces transformation.

The c-MYC proto-oncogene encodes a ubiquitous transcription factor involved in cell proliferation and tumorigenesis. Heat shock protein 60 (HSP60) plays an essential role in assisting many newly synthesized proteins to reach their native forms. Increased HSP60 expression is observed in different types of human cancer.