MAML1 promotes ESCC aggressiveness through upregulation of EMT marker TWIST1.

Forghanifard, MM; Azaraz, S; Ardalan Khales, S; Morshedi Rad, D; Abbaszadegan, MR

MAML1 promotes ESCC aggressiveness through upregulation of EMT marker TWIST1.

Forghanifard, MM Azaraz, S Ardalan Khales, S Morshedi Rad, D

Abbaszadegan, MR

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Publisher:: SPRINGER
Publication Type:: Journal Article
Citation:: Molecular biology reports, 2020, 47, (4), pp. 2659-2668
Issue Date:: 2020-04

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Field	Value	Language
dc.contributor.author	Forghanifard, MM
dc.contributor.author	Azaraz, S
dc.contributor.author	Ardalan Khales, S
dc.contributor.author	Morshedi Rad, D https://orcid.org/0000-0001-8874-4212
dc.contributor.author	Abbaszadegan, MR
dc.date.accessioned	2021-04-26T06:53:50Z
dc.date.available	2020-02-27
dc.date.available	2021-04-26T06:53:50Z
dc.date.issued	2020-04
dc.identifier.citation	Molecular biology reports, 2020, 47, (4), pp. 2659-2668
dc.identifier.issn	0301-4851
dc.identifier.issn	1573-4978
dc.identifier.uri	http://hdl.handle.net/10453/148396
dc.description.abstract	<h4>Background</h4>Mastermind-like 1 (MAML1) is the main transcriptional co-activator of Notch signaling pathway. It plays essential roles in several pathways including MEF2C, p53, Nf-кB and Wnt/β-catenin. TWIST1 is known as a regulator of epithelial mesenchymal transition (EMT), which is considered as a primary step in promotion of tumor cell metastasis. Since concomitant expression of these genes was observed in tumors, our aim in this study was to elucidate the linkage between MAML1 and TWIST1 co-overexpression in esophageal squamous cell carcinoma (ESCC).<h4>Results</h4>While MAML1 silencing significantly down-regulated TWIST1, its ectopic expression up-regulated TWIST1 expression in both mRNA and protein levels in KYSE-30 cells. Expression of mesenchymal markers was increased significantly after MAML1 and TWIST1 ectopic expression, while epithelial markers expression was significantly decreased after silencing of both genes. Concomitant protein expression of MAML1 and TWIST1 was significantly observed in ESCC patients. Enforced expression of TWIST1 had no impact on MAML1 gene expression in KYSE-30 cells.<h4>Conclusion</h4>The results clearly suggest transcriptional regulation of TWIST1 by MAML1 transcription factor in ESCC cells KYSE-30. Since TWIST1 is known as an EMT inducing marker, our results may revealed the mastermind behind TWIST1 function and introduced MAML1 as an upstream master regulator of TWIST1 and EMT in KYSE-30 cells.
dc.format	Print-Electronic
dc.language	eng
dc.publisher	SPRINGER
dc.relation.ispartof	Molecular biology reports
dc.relation.isbasedon	10.1007/s11033-020-05356-z
dc.rights	info:eu-repo/semantics/closedAccess
dc.subject	0601 Biochemistry and Cell Biology
dc.subject.classification	Biochemistry & Molecular Biology
dc.subject.mesh	Adult
dc.subject.mesh	Biomarkers, Tumor
dc.subject.mesh	Cell Line, Tumor
dc.subject.mesh	DNA-Binding Proteins
dc.subject.mesh	Epithelial-Mesenchymal Transition
dc.subject.mesh	Esophageal Neoplasms
dc.subject.mesh	Esophageal Squamous Cell Carcinoma
dc.subject.mesh	Female
dc.subject.mesh	Gene Knockdown Techniques
dc.subject.mesh	Humans
dc.subject.mesh	Male
dc.subject.mesh	Middle Aged
dc.subject.mesh	Nuclear Proteins
dc.subject.mesh	Transcription Factors
dc.subject.mesh	Twist-Related Protein 1
dc.subject.mesh	Up-Regulation
dc.subject.mesh	Cell Line, Tumor
dc.subject.mesh	Humans
dc.subject.mesh	Esophageal Neoplasms
dc.subject.mesh	DNA-Binding Proteins
dc.subject.mesh	Nuclear Proteins
dc.subject.mesh	Transcription Factors
dc.subject.mesh	Up-Regulation
dc.subject.mesh	Adult
dc.subject.mesh	Middle Aged
dc.subject.mesh	Female
dc.subject.mesh	Male
dc.subject.mesh	Gene Knockdown Techniques
dc.subject.mesh	Epithelial-Mesenchymal Transition
dc.subject.mesh	Biomarkers, Tumor
dc.subject.mesh	Twist-Related Protein 1
dc.subject.mesh	Esophageal Squamous Cell Carcinoma
dc.subject.mesh	Adult
dc.subject.mesh	Biomarkers, Tumor
dc.subject.mesh	Cell Line, Tumor
dc.subject.mesh	DNA-Binding Proteins
dc.subject.mesh	Epithelial-Mesenchymal Transition
dc.subject.mesh	Esophageal Neoplasms
dc.subject.mesh	Esophageal Squamous Cell Carcinoma
dc.subject.mesh	Female
dc.subject.mesh	Gene Knockdown Techniques
dc.subject.mesh	Humans
dc.subject.mesh	Male
dc.subject.mesh	Middle Aged
dc.subject.mesh	Nuclear Proteins
dc.subject.mesh	Transcription Factors
dc.subject.mesh	Twist-Related Protein 1
dc.subject.mesh	Up-Regulation
dc.title	MAML1 promotes ESCC aggressiveness through upregulation of EMT marker TWIST1.
dc.type	Journal Article
utslib.citation.volume	47
utslib.location.activity	Netherlands
utslib.for	0601 Biochemistry and Cell Biology
pubs.organisational-group	/University of Technology Sydney
pubs.organisational-group	/University of Technology Sydney/Faculty of Engineering and Information Technology
pubs.organisational-group	/University of Technology Sydney/Faculty of Engineering and Information Technology/School of Biomedical Engineering
utslib.copyright.status	closed_access	*
pubs.consider-herdc	false
dc.date.updated	2021-04-26T06:53:48Z
pubs.issue	4
pubs.publication-status	Published
pubs.volume	47
utslib.citation.issue	4

Abstract:

Background

Mastermind-like 1 (MAML1) is the main transcriptional co-activator of Notch signaling pathway. It plays essential roles in several pathways including MEF2C, p53, Nf-кB and Wnt/β-catenin. TWIST1 is known as a regulator of epithelial mesenchymal transition (EMT), which is considered as a primary step in promotion of tumor cell metastasis. Since concomitant expression of these genes was observed in tumors, our aim in this study was to elucidate the linkage between MAML1 and TWIST1 co-overexpression in esophageal squamous cell carcinoma (ESCC).

Results

While MAML1 silencing significantly down-regulated TWIST1, its ectopic expression up-regulated TWIST1 expression in both mRNA and protein levels in KYSE-30 cells. Expression of mesenchymal markers was increased significantly after MAML1 and TWIST1 ectopic expression, while epithelial markers expression was significantly decreased after silencing of both genes. Concomitant protein expression of MAML1 and TWIST1 was significantly observed in ESCC patients. Enforced expression of TWIST1 had no impact on MAML1 gene expression in KYSE-30 cells.

Conclusion

The results clearly suggest transcriptional regulation of TWIST1 by MAML1 transcription factor in ESCC cells KYSE-30. Since TWIST1 is known as an EMT inducing marker, our results may revealed the mastermind behind TWIST1 function and introduced MAML1 as an upstream master regulator of TWIST1 and EMT in KYSE-30 cells.

Please use this identifier to cite or link to this item:

http://hdl.handle.net/10453/148396