Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA154367 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE32694: Transcriptome and microRNA array analyses reveal a stimulatory effect of the phytochemical shikonin on epithelial–mesenchymal transition (EMT) in mouse skin [gene expression profile] GSE32695: Transcriptome and microRNA array analyses reveal a stimulatory effect of the phytochemical shikonin on epithelial–mesenchymal transition (EMT) in mouse skin [microRNA expression profile] Refer to individual Series
2011-12-31 | E-GEOD-32696 | biostudies-arrayexpress
Project description:We investigate and define here the in vivo biological effects of shikonin, at the transcriptome and microRNA levels, in mouse skin tissues. Through cross-examination between total RNA transcripts and microRNA data sets, we predicted that shikonin treatment may affect the epithelial–mesenchymal transition (EMT) process and the expression of related microRNAs, including 200a, 200b, 200c, 141, 205 and 429 microRNAs, in test skin tissue. Indeed, further in vivo tests on mouse abdominal skin tissue confirmed the stimulatory effect of shikonin on regulatory molecules of the EMT process in epidermal tissue. In addition, RT-PCR analyses confirmed the downregulating effects of shikonin on the expression of microRNA 205 and members of the microRNA 200 family, which are known to be involved in the EMT process. Gene expression of two RNA targets of the microRNA 200 family in EMT regulation, namely Sip1 (Zeb2) and Tcf8 (Zeb1), were consistently upregulated by shikonin treatment. We demonstrate here that shikonin can confer a potent stimulatory effect on the EMT process and suppress the associated-microRNAs expression in vivo in skin tissues. In order to systematically evaluate the effects of shikonin on mouse skin tissues, we next compared the gene expression profiles in shikonin-treated and acetone-treated skin tissues at different time points. Total RNA samples were collected at indicated time points for transcriptome and microRNA array analyses.
2011-12-31 | E-GEOD-32695 | biostudies-arrayexpress
Project description:We investigate and define here the in vivo biological effects of shikonin, at the transcriptome and microRNA levels, in mouse skin tissues. Through cross-examination between total RNA transcripts and microRNA data sets, we predicted that shikonin treatment may affect the epithelial–mesenchymal transition (EMT) process and the expression of related microRNAs, including 200a, 200b, 200c, 141, 205 and 429 microRNAs, in test skin tissue. Indeed, further in vivo tests on mouse abdominal skin tissue confirmed the stimulatory effect of shikonin on regulatory molecules of the EMT process in epidermal tissue. In addition, RT-PCR analyses confirmed the downregulating effects of shikonin on the expression of microRNA 205 and members of the microRNA 200 family, which are known to be involved in the EMT process. Gene expression of two RNA targets of the microRNA 200 family in EMT regulation, namely Sip1 (Zeb2) and Tcf8 (Zeb1), were consistently upregulated by shikonin treatment. We demonstrate here that shikonin can confer a potent stimulatory effect on the EMT process and suppress the associated-microRNAs expression in vivo in skin tissues. In order to systematically evaluate the effects of shikonin on mouse skin tissues, we next compared the gene expression profiles in shikonin-treated and acetone-treated skin tissues at different time points. Total RNA samples were collected at indicated time points for transcriptome and microRNA array analyses.
2011-12-31 | E-GEOD-32694 | biostudies-arrayexpress
Project description:Transcriptome and microRNA array analyses reveal a stimulatory effect of the phytochemical shikonin on epithelial–mesenchymal transition (EMT) in mouse skin
| PRJNA146889 | ENA
Project description:We investigate and define here the in vivo biological effects of shikonin, at the transcriptome and microRNA levels, in mouse skin tissues. Through cross-examination between total RNA transcripts and microRNA data sets, we predicted that shikonin treatment may affect the epithelial–mesenchymal transition (EMT) process and the expression of related microRNAs, including 200a, 200b, 200c, 141, 205 and 429 microRNAs, in test skin tissue. Indeed, further in vivo tests on mouse abdominal skin tissue confirmed the stimulatory effect of shikonin on regulatory molecules of the EMT process in epidermal tissue. In addition, RT-PCR analyses confirmed the downregulating effects of shikonin on the expression of microRNA 205 and members of the microRNA 200 family, which are known to be involved in the EMT process. Gene expression of two RNA targets of the microRNA 200 family in EMT regulation, namely Sip1 (Zeb2) and Tcf8 (Zeb1), were consistently upregulated by shikonin treatment. We demonstrate here that shikonin can confer a potent stimulatory effect on the EMT process and suppress the associated-microRNAs expression in vivo in skin tissues.
2011-12-31 | GSE32694 | GEO
Project description:We investigate and define here the in vivo biological effects of shikonin, at the transcriptome and microRNA levels, in mouse skin tissues. Through cross-examination between total RNA transcripts and microRNA data sets, we predicted that shikonin treatment may affect the epithelial–mesenchymal transition (EMT) process and the expression of related microRNAs, including 200a, 200b, 200c, 141, 205 and 429 microRNAs, in test skin tissue. Indeed, further in vivo tests on mouse abdominal skin tissue confirmed the stimulatory effect of shikonin on regulatory molecules of the EMT process in epidermal tissue. In addition, RT-PCR analyses confirmed the downregulating effects of shikonin on the expression of microRNA 205 and members of the microRNA 200 family, which are known to be involved in the EMT process. Gene expression of two RNA targets of the microRNA 200 family in EMT regulation, namely Sip1 (Zeb2) and Tcf8 (Zeb1), were consistently upregulated by shikonin treatment. We demonstrate here that shikonin can confer a potent stimulatory effect on the EMT process and suppress the associated-microRNAs expression in vivo in skin tissues.
2011-12-31 | GSE32695 | GEO
Project description:Transcriptome and microRNA array analyses reveal a stimulatory effect of the phytochemical shikonin on epithelial–mesenchymal transition (EMT) in mouse skin [gene expression profile]
| PRJNA154485 | ENA
Project description:Epithelial to Mesenchymal Transition (EMT) has been associated with cancer cell heterogeneity, plasticity and metastasis. It has been the subject of several modeling effort. This logical model of the EMT cellular network aims to assess microenvironmental signals controlling cancer-associated phenotypes amid the EMT continuum. Its outcomes relate to the qualitative degrees of cell adhesions by adherent junctions and focal adhesions, two features affected during EMT. Model attractors recover epithelial, mesenchymal and hybrid phenotypes, and simulations show that hybrid phenotypes may arise through independent molecular paths, involving stringent extrinsic signals.
Of particular interest, model predictions and their experimental validations indicated that: 1) ECM stiffening is a prerequisite for cells overactivating FAK-SRC to upregulate SNAIL1 and acquire a mesenchymal phenotype, and 2) FAK-SRC inhibition of cell-cell contacts through the Receptor Protein Tyrosine Phosphates kappa leads to the acquisition of a full mesenchymal rather than a hybrid phenotype.
2020-06-30 | MODEL2004040001 | BioModels
Project description:The present study is aimed at detecting and measuring mRNA levels of genes involved in epithelial to mesenchymal transition (EMT) in biological samples, i.e. in peripheral blood samples of colorectal cancer (CRC) patients and healthy controls, to determine the presence of disease, its progression and risk of recurrence.
| 2334276 | ecrin-mdr-crc
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