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Twist1 regulates stem cell properties in mesenchymal stem cells

ABSTRACT: To investigate the function TWIST1 in the regulation of stemness in mesenchymal stem cell, we established human mesenchymal stem cell in TWIST1-overexpression.

ORGANISM(S): Homo sapiens

PROVIDER: GSE232324 | GEO | 2023/05/16

REPOSITORIES: GEO

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Twist1 regulates stem cell properties in mesenchymal stem cells

Project description:To investigate the function TWIST1 in the regulation of stemness in mesenchymal stem cell, we established human mesenchymal stem cell in TWIST1-overexpression.

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Twist1 regulates stem cell properties in mesenchymal stem cells

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Project description:It is well known that the properties of hematopoietic stem cells (HSCs) such as their ability to self-renew, and multipotency are maintained through interactions with mesenchymal cells. Meanwhile, the identification of cells that are the key component of niche remains a subject of dispute. Mesenchymal stem cells (MSCs) are one of the niche component cells, MSCs are one of the niche component cells which provide stemness signal to HSCs, while it is also hypothesized that there is also a counterpart signal from hematopoiesistic cells to mesenchymeal cells, as HSCs also constitute core stem cells niche for MSCs. Although mesenchymal stem cells (MSCs) have also been studied intensively, the signals involved in the maintenance of their properties have not attracted much attentions. We used microarrays to detail the global programme of gene expression underlying HSC-MSC interaction and identified distinct classes of regulated genes during this process.

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TWIST1-induced microRNA-424 drives an intermediate epithelial-to-mesenchymal transition that opposes metastasis

Project description:Epithelial-to-mesenchymal transition (EMT) is a dynamic process that relies on cellular plasticity; an EMT/MET axis is critical for metastatic colonization of carcinomas. Unlike epithelial programming, regulation of mesenchymal programming is not well understood in EMT. Here we describe the first microRNA that enhances exclusively mesenchymal programming. We demonstrate that microRNA-424 is up-regulated early during a TWIST1/SNAI1-induced EMT, and that it causes cells to express mesenchymal genes without affecting epithelial genes, resulting in a mixed/intermediate EMT. Further, microRNA-424 increases motility, decreases adhesion and induces a growth arrest, changes associated with a complete EMT. Patient microRNA-424 levels positively associate with TWIST1/2 and EMT-like gene signatures and is increased in primary tumors versus matched normal breast. However, microRNA-424 is down-regulated in metastases versus matched primary tumors. Correspondingly, microRNA-424 decreases tumor initiation and is post-transcriptionally down-regulated in macrometastases in mice. RNA-seq identified microRNA-424 regulates numerous genes associated with EMT and breast cancer stemness including the novel miR-424 target, TGFBR3, which regulates mesenchymal phenotypes without influencing miR-424 effects on tumor-initiating phenotypes; instead, we show that ERK signaling is critical for such tumor-initiating effects of miR-424. These findings suggest microRNA-424 plays distinct roles downstream of EMT-inducing factors, facilitating earlier stages, but repressing later stages, of metastasis. Examination of mRNA levels in MCF12A human breast cell lines that stably over-expressed miR-424 or an empty vector (EV) control. Each group has three replicates.

2015-02-26 | E-GEOD-54505 | biostudies-arrayexpress

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