Identification of EMT signaling cross-talk and gene regulatory networks by single-cell RNA sequencing
The epithelial-to-mesenchymal transition (EMT) plays a critical role during normal development and in cancer progression. EMT is induced by various signaling pathways, including TGF-β, BMP, Wnt-β-catenin, NOTCH, Shh, and receptor tyrosine kinases. In this study, we performed single-cell RNA sequenci...
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| Vydané v: | Proceedings of the National Academy of Sciences - PNAS Ročník 118; číslo 19 |
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| Hlavní autori: | , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | English |
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11.05.2021
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| ISSN: | 1091-6490, 1091-6490 |
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| Abstract | The epithelial-to-mesenchymal transition (EMT) plays a critical role during normal development and in cancer progression. EMT is induced by various signaling pathways, including TGF-β, BMP, Wnt-β-catenin, NOTCH, Shh, and receptor tyrosine kinases. In this study, we performed single-cell RNA sequencing on MCF10A cells undergoing EMT by TGF-β1 stimulation. Our comprehensive analysis revealed that cells progress through EMT at different paces. Using pseudotime clustering reconstruction of gene-expression profiles during EMT, we found sequential and parallel activation of EMT signaling pathways. We also observed various transitional cellular states during EMT. We identified regulatory signaling nodes that drive EMT with the expression of important microRNAs and transcription factors. Using a random circuit perturbation methodology, we demonstrate that the NOTCH signaling pathway acts as a key driver of TGF-β-induced EMT. Furthermore, we demonstrate that the gene signatures of pseudotime clusters corresponding to the intermediate hybrid EMT state are associated with poor patient outcome. Overall, this study provides insight into context-specific drivers of cancer progression and highlights the complexities of the EMT process. |
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| AbstractList | The epithelial-to-mesenchymal transition (EMT) plays a critical role during normal development and in cancer progression. EMT is induced by various signaling pathways, including TGF-β, BMP, Wnt-β-catenin, NOTCH, Shh, and receptor tyrosine kinases. In this study, we performed single-cell RNA sequencing on MCF10A cells undergoing EMT by TGF-β1 stimulation. Our comprehensive analysis revealed that cells progress through EMT at different paces. Using pseudotime clustering reconstruction of gene-expression profiles during EMT, we found sequential and parallel activation of EMT signaling pathways. We also observed various transitional cellular states during EMT. We identified regulatory signaling nodes that drive EMT with the expression of important microRNAs and transcription factors. Using a random circuit perturbation methodology, we demonstrate that the NOTCH signaling pathway acts as a key driver of TGF-β-induced EMT. Furthermore, we demonstrate that the gene signatures of pseudotime clusters corresponding to the intermediate hybrid EMT state are associated with poor patient outcome. Overall, this study provides insight into context-specific drivers of cancer progression and highlights the complexities of the EMT process.The epithelial-to-mesenchymal transition (EMT) plays a critical role during normal development and in cancer progression. EMT is induced by various signaling pathways, including TGF-β, BMP, Wnt-β-catenin, NOTCH, Shh, and receptor tyrosine kinases. In this study, we performed single-cell RNA sequencing on MCF10A cells undergoing EMT by TGF-β1 stimulation. Our comprehensive analysis revealed that cells progress through EMT at different paces. Using pseudotime clustering reconstruction of gene-expression profiles during EMT, we found sequential and parallel activation of EMT signaling pathways. We also observed various transitional cellular states during EMT. We identified regulatory signaling nodes that drive EMT with the expression of important microRNAs and transcription factors. Using a random circuit perturbation methodology, we demonstrate that the NOTCH signaling pathway acts as a key driver of TGF-β-induced EMT. Furthermore, we demonstrate that the gene signatures of pseudotime clusters corresponding to the intermediate hybrid EMT state are associated with poor patient outcome. Overall, this study provides insight into context-specific drivers of cancer progression and highlights the complexities of the EMT process. The epithelial-to-mesenchymal transition (EMT) plays a critical role during normal development and in cancer progression. EMT is induced by various signaling pathways, including TGF-β, BMP, Wnt-β-catenin, NOTCH, Shh, and receptor tyrosine kinases. In this study, we performed single-cell RNA sequencing on MCF10A cells undergoing EMT by TGF-β1 stimulation. Our comprehensive analysis revealed that cells progress through EMT at different paces. Using pseudotime clustering reconstruction of gene-expression profiles during EMT, we found sequential and parallel activation of EMT signaling pathways. We also observed various transitional cellular states during EMT. We identified regulatory signaling nodes that drive EMT with the expression of important microRNAs and transcription factors. Using a random circuit perturbation methodology, we demonstrate that the NOTCH signaling pathway acts as a key driver of TGF-β-induced EMT. Furthermore, we demonstrate that the gene signatures of pseudotime clusters corresponding to the intermediate hybrid EMT state are associated with poor patient outcome. Overall, this study provides insight into context-specific drivers of cancer progression and highlights the complexities of the EMT process. |
| Author | Arslan, Emre Rai, Kunal Jolly, Mohit Kumar Mani, Sendurai A Levine, Herbert Deshmukh, Abhijeet P Vasaikar, Suhas V den Hollander, Petra Soundararajan, Rama Tomczak, Katarzyna Tripathi, Shubham Chakraborty, Priyanka |
| Author_xml | – sequence: 1 givenname: Abhijeet P orcidid: 0000-0002-3587-8812 surname: Deshmukh fullname: Deshmukh, Abhijeet P organization: Department of Translational Molecular Pathology, University of Texas MD Anderson Cancer Center, Houston, TX 77030 – sequence: 2 givenname: Suhas V surname: Vasaikar fullname: Vasaikar, Suhas V organization: Department of Translational Molecular Pathology, University of Texas MD Anderson Cancer Center, Houston, TX 77030 – sequence: 3 givenname: Katarzyna orcidid: 0000-0003-0553-8056 surname: Tomczak fullname: Tomczak, Katarzyna organization: Department of Genomic Medicine, University of Texas MD Anderson Cancer Center, Houston, TX 77030 – sequence: 4 givenname: Shubham orcidid: 0000-0002-0141-987X surname: Tripathi fullname: Tripathi, Shubham organization: Center for Theoretical Biological Physics, Northeastern University, Boston, MA 02115 – sequence: 5 givenname: Petra surname: den Hollander fullname: den Hollander, Petra organization: Department of Translational Molecular Pathology, University of Texas MD Anderson Cancer Center, Houston, TX 77030 – sequence: 6 givenname: Emre surname: Arslan fullname: Arslan, Emre organization: Department of Genomic Medicine, University of Texas MD Anderson Cancer Center, Houston, TX 77030 – sequence: 7 givenname: Priyanka surname: Chakraborty fullname: Chakraborty, Priyanka organization: Centre for BioSystems Science and Engineering, Indian Institute of Science, 560012 Bangalore, India – sequence: 8 givenname: Rama orcidid: 0000-0001-6976-3784 surname: Soundararajan fullname: Soundararajan, Rama organization: Department of Translational Molecular Pathology, University of Texas MD Anderson Cancer Center, Houston, TX 77030 – sequence: 9 givenname: Mohit Kumar orcidid: 0000-0002-6631-2109 surname: Jolly fullname: Jolly, Mohit Kumar organization: Centre for BioSystems Science and Engineering, Indian Institute of Science, 560012 Bangalore, India – sequence: 10 givenname: Kunal surname: Rai fullname: Rai, Kunal email: krai@mdanderson.org, h.levine@northeastern.edu, Smani@mdanderson.org organization: Department of Genomic Medicine, University of Texas MD Anderson Cancer Center, Houston, TX 77030; krai@mdanderson.org h.levine@northeastern.edu Smani@mdanderson.org – sequence: 11 givenname: Herbert orcidid: 0000-0002-8819-9055 surname: Levine fullname: Levine, Herbert email: krai@mdanderson.org, h.levine@northeastern.edu, Smani@mdanderson.org organization: Department of Physics, Northeastern University, Boston, MA 02115 – sequence: 12 givenname: Sendurai A orcidid: 0000-0002-5918-4276 surname: Mani fullname: Mani, Sendurai A email: krai@mdanderson.org, h.levine@northeastern.edu, Smani@mdanderson.org organization: Department of Translational Molecular Pathology, University of Texas MD Anderson Cancer Center, Houston, TX 77030; krai@mdanderson.org h.levine@northeastern.edu Smani@mdanderson.org |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/33941680$$D View this record in MEDLINE/PubMed |
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| Title | Identification of EMT signaling cross-talk and gene regulatory networks by single-cell RNA sequencing |
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