A drive in SUVs: From development to disease

Rao, Vinay Kumar; Pal, Ananya; Taneja, Reshma

doi:10.1080/15592294.2017.1281502

Cited by 49 publications

(38 citation statements)

References 113 publications

(148 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…One of the major KMT families that introduce transcriptional repression is the SUV39 sub-family, including SUV39H2 (KMT1B), G9a (EHMT2), G9a-like protein1, GLP (EHMT1), SETDB1 (KMT1E), and SETDB2 (KMT1F) [ 4 ], among which SUV39H1 and SUV39H2 can preferentially read H3K9me1 via their chromodomain and catalyze H3K9me3 [ 5 – 7 ]. Moreover, SUV39H1 and SUV39H2 exert mutually compensated expression throughout the embryonic development, implying a functional redundancy between the two enzymes [ 8 ].…”

Section: Introductionmentioning

confidence: 99%

Identification of SUV39H2 as a potential oncogene in lung adenocarcinoma

Zheng

Wang

et al. 2018

Clin Epigenet

View full text Add to dashboard Cite

BackgroundSUV39H2 (suppressor of variegation 3-9 homolog 2), which introduces H3K9me3 to induce transcriptional repression, has been reported to play critical roles in heterochromatin maintenance, DNA repair, and recently, carcinogenesis. Dysregulation of SUV39H2 expression has been observed in several types of cancers. However, neither the genomic landscape nor the clinical significance of SUV39H2 in lung adenocarcinoma has been probed comprehensively.MethodsIn this research, we conducted bioinformatics analysis to primarily sort out potential genes with dysregulated expressions. After we identified SUV39H2, RNA-seq was performed for a high-throughput evaluation of altered gene expression and dysregulated pathways, followed by a series of validations via RT-qPCR and bioinformatics analyses. Finally, to assess the potential oncogenic role of SUV39H2, we employed the invasion assay and clone formation assay in vitro and tumorigenesis assays in mouse models in vivo.ResultsThrough bioinformatics analyses, we found that SUV39H2 underwent a severe upregulation in the tumor tissue, which was also confirmed in the surgically removed tissues. Overexpression of SUV39H2 was mainly associated with its amplification and with shorter patient overall survival. Then, the RNA-seq demonstrated that TPM4, STOM, and OPTN might be affected by the loss of function of SUV39H2. Finally, in vitro and in vivo experiments with SUV39H2 knockdown all suggested a potential role of SUV39H2 in both carcinogenesis and metastasis.ConclusionsSUV39H2 expression was elevated in lung adenocarcinoma. TPM4, OPTN, and STOM were potentially regulated by SUV39H2. SUV39H2 might be a potential oncogene in lung adenocarcinoma, mediating tumorigenesis and metastasis.Electronic supplementary materialThe online version of this article (10.1186/s13148-018-0562-4) contains supplementary material, which is available to authorized users.

show abstract

Section: Introductionmentioning

confidence: 99%

Identification of SUV39H2 as a potential oncogene in lung adenocarcinoma

Zheng

Wang

et al. 2018

Clin Epigenet

View full text Add to dashboard Cite

show abstract

“…[78][79][80] Of significance, in this study, miR24-2 enhances Pim1 [92][93][94] and lysine methyltransferases SUV39H1 and Nanog regulate several oncogene expression in various cancer cells. 95,96 Recent work has provided a fact that the activation, regulation, and functions of MEKK kinases and tyrosine phosphorylation in several cancers. 97,98 Therefore, miR24-2 may play an important role through these related genes during hepatocarcinogenesis.…”

Section: Discussionmentioning

confidence: 99%

miR24‐2 accelerates progression of liver cancer cells by activating Pim1 through tri‐methylation of Histone H3 on the ninth lysine

Yang

Song

Meng

et al. 2020

J Cellular Molecular Medi

View full text Add to dashboard Cite

Several microRNAs are associated with carcinogenesis and tumour progression. Herein, our observations suggest both miR24‐2 and Pim1 are up‐regulated in human liver cancers, and miR24‐2 accelerates growth of liver cancer cells in vitro and in vivo. Mechanistically, miR24‐2 increases the expression of N6‐adenosine‐methyltransferase METTL3 and thereafter promotes the expression of miR6079 via RNA methylation modification. Furthermore, miR6079 targets JMJD2A and then increased the tri‐methylation of histone H3 on the ninth lysine (H3K9me3). Therefore, miR24‐2 inhibits JMJD2A by increasing miR6079 and then increases H3K9me3. Strikingly, miR24‐2 increases the expression of Pim1 dependent on H3K9me3 and METTL3. Notably, our findings suggest that miR24‐2 alters several related genes (pHistone H3, SUZ12, SUV39H1, Nanog, MEKK4, pTyr) and accelerates progression of liver cancer cells through Pim1 activation. In particular, Pim1 is required for the oncogenic action of miR24‐2 in liver cancer. This study elucidates a novel mechanism for miR24‐2 in liver cancer and suggests that miR24‐2 may be used as novel therapeutic targets of liver cancer.

show abstract

“…Suppressor of variegation 3-9 homolog 2 (SUV39H2, also known as KMT1B) is a member of the SUV39 subfamily of lysine methyltransferases (KMTs) and is known to be localized in nucleus; it is the second H3K9 selective methyltransferases recognized after its homolog SUV39H1 [1,2]. In humans, the SUV39 family proteins, namely SUV39H1 (KMT1A), SUV39H2 (KMT1B), SETDB1 (KMT1E), SETDB2 (KMT1F), G9A (EHMT2) and G9a-like protein (GLP1), contain pre-SET (N-SET) and post-SET (C-SET) domains besides the SET domain and mediate H3K9 methylation [3][4][5][6]. SUV39H2 is primarily responsible for di-and tri-methylation of H3K9; H3K9me3 is associated with heterochromatin organization at pericentric and telomeric repeats, transcriptional repression, and epigenetic silencing of the domains in euchromatin [1,[7][8][9][10][11][12].…”

Section: Introductionmentioning

confidence: 99%

The Oncogenic Potential of SUV39H2: A Comprehensive and Perspective View

Li¹,

Zheng²,

Yang³

2019

J. Cancer

View full text Add to dashboard Cite

Epigenetic modifications at the histone level have attracted significant attention because of their roles in tumorigenesis. Suppressor of variegation 3-9 homolog 2 (SUV39H2, also known as KMT1B) is a member of the SUV39 subfamily of lysine methyltransferases (KMTs) that plays a significant role in histone H3-K9 di-/tri-methylation, transcriptional regulation and cell cycle. Overexpressions of SUV39H2 at gene, mRNA and protein levels are known to be associated with a range of cancers: leukemia, lymphomas, lung cancer, breast cancer, colorectal cancer, gastric cancer, hepatocellular cancer and so on. Accumulating evidence indicates that SUV39H2 acts as an oncogene and contributes to the initiation and progression of cancers. It could, therefore, be a promising target for anti-cancer treatment. In this review, we focus on the dysregulation of SUV39H2 in cancers, including its clinical prognostic predictor role, molecular mechanism involved in cancer occurrence and development, relevant inhibitors against cancer, and its epigenetic modification interaction with immunotherapy. A better understanding of the SUV39H2 will be beneficial to the development of molecular-targeted therapies in cancer.

show abstract

A drive in SUVs: From development to disease

Cited by 49 publications

References 113 publications

Identification of SUV39H2 as a potential oncogene in lung adenocarcinoma

Identification of SUV39H2 as a potential oncogene in lung adenocarcinoma

miR24‐2 accelerates progression of liver cancer cells by activating Pim1 through tri‐methylation of Histone H3 on the ninth lysine

The Oncogenic Potential of SUV39H2: A Comprehensive and Perspective View

Contact Info

Product

Resources

About