Transcriptome and microRNA array analyses reveal a stimulatory effect of the phytochemical shikonin on epithelial–mesenchymal transition (EMT) in mouse skin
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE32696 | GEO | 2011/12/31
SECONDARY ACCESSION(S): PRJNA146889
REPOSITORIES: GEO
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.
2011-12-31 | GSE32695 | 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 | 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. 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:Although various pharmacological activities of the shikonins have been documented, understanding the hierarchical regulation of these diverse bioactivities at the genome level is unsubstantiated. In this study, through cross examination between transcriptome and microRNA array analyses, we predicted that topical treatment of shikonin in vivo affects epithelial-mesenchymal transition (EMT) and the expression of related microRNAs, including 200a, 200b, 200c, 141, 205, and 429 microRNAs, in mouse skin tissues. In situ immunohistological analyses further demonstrated that specific EMT regulatory molecules are enhanced in shikonin-treated epidermal tissues. RT-PCR analyses subsequently confirmed that shikonin treatment downregulated expression of microRNA-205 and other members of the 200 family microRNAs. Further, expression of two RNA targets of the 200 family microRNAs in EMT regulation, Sip1 (Zeb2) and Tcf8 (Zeb1), was consistently upregulated by shikonin treatment. Enhancement of these EMT activities was also detected in shikonin-treated wounds, which repaired faster than controls. These results suggest that topical treatment with shikonin can confer a potent stimulatory effect on EMT and suppress the expression of the associated microRNAs in skin wound healing. Collectively, these cellular and molecular data provide further evidence in support of our previous findings on the specific pharmacological effects of shikonin in wound healing and immune modulation.
| S-EPMC3686062 | biostudies-literature
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:The origin of myofibroblasts in fibrotic conditions remains unknown and in systemic sclerosis (SSc) it has been proposed that activation of local fibroblasts, trans-differentiation of perivascular or vascular cells, recruitment of fibrocyte progenitors, or epithelial to mesenchymal transition (EMT) could be contributing. Data from our laboratory indicate that the epidermis in scleroderma is activated with the keratinocytes exhibiting a phenotype normally associated with tissue repair, including phosphorylation profiles indicative of TGFβ signaling. Since TGFβ is a known inducer of EMT, we investigated if there is evidence of this process in the SSc epidermis. In order to validate antibodies and primers, EMT was modeled in HaCaT cells cultured in the presence of TGFβ1. Skin sections were stained with phosho-SMAD2/3, as well as with epithelial and mesenchymal markers. Moreover, mRNA levels of transcription factors associated with EMT were studied in epidermal blister sheets. We observed critical changes in the scleroderma epidermis; showing significantly increased nuclear translocation of phosphorylated Smad2/3, consistent with active TGFβ signaling in SSc keratinocytes. While profound EMT could be induced in keratinocytes in vitro with the appearance of SNAI1/2 and FSP-1, and an accompanying loss of E-cadherin, in the scleroderma skin active TGFβ signaling was accompanied by only partial EMT-like changes characterised by induction of SNAI1 alone and with no loss of E-cadherin. Together, our findings support a model of altered differentiation and TGFβ dependent activation of scleroderma epithelial cells leading to a partially evoked EMT like process in the fibrotic skin.
| S-EPMC4517793 | biostudies-literature
Project description:Constitutive heterochromatin, an essential structure that has been conserved throughout evolution, is required to maintain genome stability. Although heterochromatin is enriched for repressive traits, it can be actively transcribed to generate thousands of noncoding RNAs that are required for correct chromatin assembly. Despite the importance of this structure, how and why heterochromatin transcription is regulated, and the proteins responsible for this regulation, remain poorly understood. Here, we summarize recent findings in heterochromatin transcription regulation during different cellular processes with a focus on the epithelial-mesenchymal transition (EMT), which elicits important changes in cell behavior, has a key role in early development, and is involved in cancer progression.
| S-EPMC4905179 | biostudies-other
Project description:Therapy resistance is a characteristic of cancer cells that significantly reduces the effectiveness of drugs. Despite the popularity of cisplatin (CP) as a chemotherapeutic agent, which is widely used in the treatment of various types of cancer, resistance of cancer cells to CP chemotherapy has been extensively observed. Among various reported mechanism(s), the epithelial-mesenchymal transition (EMT) process can significantly contribute to chemoresistance by converting the motionless epithelial cells into mobile mesenchymal cells and altering cell-cell adhesion as well as the cellular extracellular matrix, leading to invasion of tumor cells. By analyzing the impact of the different molecular pathways such as microRNAs, long non-coding RNAs, nuclear factor-?B (NF-?B), phosphoinositide 3-kinase-related protein kinase (PI3K)/Akt, mammalian target rapamycin (mTOR), and Wnt, which play an important role in resistance exhibited to CP therapy, we first give an introduction about the EMT mechanism and its role in drug resistance. We then focus specifically on the molecular pathways involved in drug resistance and the pharmacological strategies that can be used to mitigate this resistance. Overall, we highlight the various targeted signaling pathways that could be considered in future studies to pave the way for the inhibition of EMT-mediated resistance displayed by tumor cells in response to CP exposure.
| S-EPMC7312011 | biostudies-literature