2020
DOI: 10.2147/ott.s259873
|View full text |Cite
|
Sign up to set email alerts
|

<p>The Role of Methyltransferase NSD2 as a Potential Oncogene in Human Solid Tumors</p>

Abstract: Malignant solid tumors are the leading cause of death in humans, and epigenetic regulation plays a significant role in studying the mechanism of human solid tumors. Recently, histone lysine methylation has been demonstrated to be involved in the development of human solid tumors due to its epigenetic stability and some other advantages. The 90-kb protein methyltransferase nuclear receptor SET domain-containing 2 (NSD2) is a member of nuclear receptor SET domain-containing (NSD) protein lysine methyltransferase… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
3
1

Citation Types

0
25
0

Year Published

2020
2020
2024
2024

Publication Types

Select...
9

Relationship

0
9

Authors

Journals

citations
Cited by 20 publications
(25 citation statements)
references
References 69 publications
(84 reference statements)
0
25
0
Order By: Relevance
“…Owing to its potent role in epigenetic regulation, NSD2 has been reported to play important roles in human solid tumors by regulating DNA damage repair and epithelial–mesenchymal transition process [ 27 ]. During tumor growth, reprogrammed glucose metabolism is involved to meet the demand of glycolytic intermediates for macromolecule biosynthesis, during which the NSD2 has been reported to play a role by regulating key glucose metabolism regulators, such as TIGAR, HK2, and G6PD [ 28 ].…”
Section: Discussionmentioning
confidence: 99%
“…Owing to its potent role in epigenetic regulation, NSD2 has been reported to play important roles in human solid tumors by regulating DNA damage repair and epithelial–mesenchymal transition process [ 27 ]. During tumor growth, reprogrammed glucose metabolism is involved to meet the demand of glycolytic intermediates for macromolecule biosynthesis, during which the NSD2 has been reported to play a role by regulating key glucose metabolism regulators, such as TIGAR, HK2, and G6PD [ 28 ].…”
Section: Discussionmentioning
confidence: 99%
“…This overexpression is associated with poor prognosis and recurrence. 43 These findings reveal the qualitative relationship between genetic variation of HMT and its downstream effect, especially for oncogenes and tumor suppressor genes, which have been critical for prevention, diagnosis, and treatment of cancer. All of the HMTs presented here could be a potential panel of prognostic biomarker, especially the HMTs encoded for PRDM9, SETDB1, PRDM14, EHMT2, and NSD3 genes.…”
mentioning
confidence: 92%
“…Moreover, lower levels of NSD2 caused a higher expression of the E-cadherin protein and decreased N-cadherin as well as vimentin. NSD2 interacts with TWIST1 and causes upregulation of H3K36me2, which, in turn, is manifested with EMT promotion [ 103 ].…”
Section: Discussionmentioning
confidence: 99%