Novel molecular targets in gastric adenocarcinoma.

Ramezankhani, R; Solhi, R; Es, HA; Vosough, M; Hassan, M

Novel molecular targets in gastric adenocarcinoma.

Ramezankhani, R Solhi, R Es, HA Vosough, M Hassan, M

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Publisher:: Elsevier BV
Publication Type:: Journal Article
Citation:: Pharmacol Ther, 2021, 220, pp. 107714
Issue Date:: 2021-04

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Field	Value	Language
dc.contributor.author	Ramezankhani, R
dc.contributor.author	Solhi, R
dc.contributor.author	Es, HA
dc.contributor.author	Vosough, M
dc.contributor.author	Hassan, M
dc.date.accessioned	2022-07-04T21:21:50Z
dc.date.available	2020-10-19
dc.date.available	2022-07-04T21:21:50Z
dc.date.issued	2021-04
dc.identifier.citation	Pharmacol Ther, 2021, 220, pp. 107714
dc.identifier.issn	0163-7258
dc.identifier.issn	1879-016X
dc.identifier.uri	http://hdl.handle.net/10453/158620
dc.description.abstract	Gastric adenocarcinoma (GAC) is the third leading cause of cancer-related death worldwide. A high mortality rate and resistance to treatment protocols due to a heterogeneous molecular pathogenesis has made discovering the key etiologic molecular alterations of the utmost importance. The remarkable role played by epigenetic modifications in repressing or activating many cancer-related genes and forming new epigenetic signatures can affect cancer initiation and progression. Hence, targeting the key epigenetic drivers could potentially attenuate cancer progression. MLLs, ARID1A and EZH2 are among the major epigenetic players that are frequently mutated in GACs. In this paper, we have proposed the existence of a network between these proteins that, together with PCAF and KDM6A, control the 3D chromatin structure and regulate the expression of tumor suppressor genes (TSGs) and oncogenes in GAC. Therefore, we suggest that manipulating the expression of EZH2, PCAF, and KDM6A or their downstream targets may reduce the cancerous phenotype in GAC.
dc.format	Print-Electronic
dc.language	eng
dc.publisher	Elsevier BV
dc.relation.ispartof	Pharmacol Ther
dc.relation.isbasedon	10.1016/j.pharmthera.2020.107714
dc.rights	info:eu-repo/semantics/openAccess
dc.subject	1115 Pharmacology and Pharmaceutical Sciences
dc.subject.classification	Pharmacology & Pharmacy
dc.subject.mesh	Adenocarcinoma
dc.subject.mesh	Epigenesis, Genetic
dc.subject.mesh	Histone Demethylases
dc.subject.mesh	Humans
dc.subject.mesh	Stomach Neoplasms
dc.subject.mesh	Humans
dc.subject.mesh	Adenocarcinoma
dc.subject.mesh	Stomach Neoplasms
dc.subject.mesh	Epigenesis, Genetic
dc.subject.mesh	Histone Demethylases
dc.title	Novel molecular targets in gastric adenocarcinoma.
dc.type	Journal Article
utslib.citation.volume	220
utslib.location.activity	England
utslib.for	1115 Pharmacology and Pharmaceutical Sciences
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	open_access	*
dc.date.updated	2022-07-04T21:21:48Z
pubs.publication-status	Published
pubs.volume	220

Abstract:

Gastric adenocarcinoma (GAC) is the third leading cause of cancer-related death worldwide. A high mortality rate and resistance to treatment protocols due to a heterogeneous molecular pathogenesis has made discovering the key etiologic molecular alterations of the utmost importance. The remarkable role played by epigenetic modifications in repressing or activating many cancer-related genes and forming new epigenetic signatures can affect cancer initiation and progression. Hence, targeting the key epigenetic drivers could potentially attenuate cancer progression. MLLs, ARID1A and EZH2 are among the major epigenetic players that are frequently mutated in GACs. In this paper, we have proposed the existence of a network between these proteins that, together with PCAF and KDM6A, control the 3D chromatin structure and regulate the expression of tumor suppressor genes (TSGs) and oncogenes in GAC. Therefore, we suggest that manipulating the expression of EZH2, PCAF, and KDM6A or their downstream targets may reduce the cancerous phenotype in GAC.

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http://hdl.handle.net/10453/158620