A “NOTCH” Deeper into the Epithelial-To-Mesenchymal Transition (EMT) Program in Breast Cancer
Notch signaling is a primitive signaling pathway having various roles in the normal origin and development of each multicellular organisms. Therefore, any aberration in the pathway will inevitably lead to deadly outcomes such as cancer. It has now been more than two decades since Notch was acknowled...
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doaj-798e3ff60e714f2facdef60fa31ef4052020-11-25T01:25:19ZengMDPI AGGenes2073-44252019-11-01101296110.3390/genes10120961genes10120961A “NOTCH” Deeper into the Epithelial-To-Mesenchymal Transition (EMT) Program in Breast CancerRohan Kar0Niraj Kumar Jha1Saurabh Kumar Jha2Ankur Sharma3Sunny Dholpuria4Nidhi Asthana5Kundan Chaurasiya6Vivek Kumar Singh7Shuaib Burgee8Parma Nand9Indian Institute of Management Ahmedabad (IIMA), Gujarat 380015, IndiaDepartment of Biotechnology, School of Engineering & Technology (SET), Sharda University, Greater Noida 201306, IndiaDepartment of Biotechnology, School of Engineering & Technology (SET), Sharda University, Greater Noida 201306, IndiaDepartment of Life Science, School of Basic Science & Research (SBSR), Sharda University, Greater Noida 201306, IndiaDepartment of Life Science, School of Basic Science & Research (SBSR), Sharda University, Greater Noida 201306, IndiaNational Centre of Experimental Mineralogy & Petrology (NCEMP), University of Allahabad, Prayagraj 2l1002, IndiaDepartment of Biotechnology, School of Engineering & Technology (SET), Sharda University, Greater Noida 201306, IndiaDepartment of Biotechnology, School of Engineering & Technology (SET), Sharda University, Greater Noida 201306, IndiaDepartment of Life Science, School of Basic Science & Research (SBSR), Sharda University, Greater Noida 201306, IndiaDepartment of Biotechnology, School of Engineering & Technology (SET), Sharda University, Greater Noida 201306, IndiaNotch signaling is a primitive signaling pathway having various roles in the normal origin and development of each multicellular organisms. Therefore, any aberration in the pathway will inevitably lead to deadly outcomes such as cancer. It has now been more than two decades since Notch was acknowledged as an oncogene in mouse mammary tumor virus-infected mice. Since that discovery, activated Notch signaling and consequent up-regulation of tumor-promoting Notch target genes have been observed in human breast cancer. Moreover, consistent over-expression of Notch ligands and receptors has been shown to correlate with poor prognosis in human breast cancer. Notch regulates a number of key processes during breast carcinogenesis, of which, one key phenomenon is epithelial−mesenchymal transition (EMT). EMT is a key process for large-scale cell movement during morphogenesis at the time of embryonic development. Cancer cells aided by transcription factors usurp this developmental program to execute the multi-step process of tumorigenesis and metastasis. In this review, we recapitulate recent progress in breast cancer research that has provided new perceptions into the molecular mechanisms behind Notch-mediated EMT regulation during breast tumorigenesis.https://www.mdpi.com/2073-4425/10/12/961notchemtbreast cancermetastasisinvasionsignaling pathwayhypoxiacytokinepi3k/akt |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Rohan Kar Niraj Kumar Jha Saurabh Kumar Jha Ankur Sharma Sunny Dholpuria Nidhi Asthana Kundan Chaurasiya Vivek Kumar Singh Shuaib Burgee Parma Nand |
spellingShingle |
Rohan Kar Niraj Kumar Jha Saurabh Kumar Jha Ankur Sharma Sunny Dholpuria Nidhi Asthana Kundan Chaurasiya Vivek Kumar Singh Shuaib Burgee Parma Nand A “NOTCH” Deeper into the Epithelial-To-Mesenchymal Transition (EMT) Program in Breast Cancer Genes notch emt breast cancer metastasis invasion signaling pathway hypoxia cytokine pi3k/akt |
author_facet |
Rohan Kar Niraj Kumar Jha Saurabh Kumar Jha Ankur Sharma Sunny Dholpuria Nidhi Asthana Kundan Chaurasiya Vivek Kumar Singh Shuaib Burgee Parma Nand |
author_sort |
Rohan Kar |
title |
A “NOTCH” Deeper into the Epithelial-To-Mesenchymal Transition (EMT) Program in Breast Cancer |
title_short |
A “NOTCH” Deeper into the Epithelial-To-Mesenchymal Transition (EMT) Program in Breast Cancer |
title_full |
A “NOTCH” Deeper into the Epithelial-To-Mesenchymal Transition (EMT) Program in Breast Cancer |
title_fullStr |
A “NOTCH” Deeper into the Epithelial-To-Mesenchymal Transition (EMT) Program in Breast Cancer |
title_full_unstemmed |
A “NOTCH” Deeper into the Epithelial-To-Mesenchymal Transition (EMT) Program in Breast Cancer |
title_sort |
“notch” deeper into the epithelial-to-mesenchymal transition (emt) program in breast cancer |
publisher |
MDPI AG |
series |
Genes |
issn |
2073-4425 |
publishDate |
2019-11-01 |
description |
Notch signaling is a primitive signaling pathway having various roles in the normal origin and development of each multicellular organisms. Therefore, any aberration in the pathway will inevitably lead to deadly outcomes such as cancer. It has now been more than two decades since Notch was acknowledged as an oncogene in mouse mammary tumor virus-infected mice. Since that discovery, activated Notch signaling and consequent up-regulation of tumor-promoting Notch target genes have been observed in human breast cancer. Moreover, consistent over-expression of Notch ligands and receptors has been shown to correlate with poor prognosis in human breast cancer. Notch regulates a number of key processes during breast carcinogenesis, of which, one key phenomenon is epithelial−mesenchymal transition (EMT). EMT is a key process for large-scale cell movement during morphogenesis at the time of embryonic development. Cancer cells aided by transcription factors usurp this developmental program to execute the multi-step process of tumorigenesis and metastasis. In this review, we recapitulate recent progress in breast cancer research that has provided new perceptions into the molecular mechanisms behind Notch-mediated EMT regulation during breast tumorigenesis. |
topic |
notch emt breast cancer metastasis invasion signaling pathway hypoxia cytokine pi3k/akt |
url |
https://www.mdpi.com/2073-4425/10/12/961 |
work_keys_str_mv |
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