SUV420H2 is an epigenetic regulator of epithelial/mesenchymal states in pancreatic cancer

Viotti, Manuel; Wilson, Catherine; McCleland, Mark L.; Koeppen, Hartmut; Haley, Benjamin; Jhunjhunwala, Suchit; Klijn, Christiaan; Modrušan, Zora; Arnott, David; Classon, Marie; Stéphan, Jean-Philippe; Mellman, Ira

doi:10.1083/jcb.201705031

Cited by 37 publications

(36 citation statements)

References 70 publications

(95 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…SUV420H2 induces silencing of key drivers of epithelial cell identity, such as HNF4α and FoxA1, and its attenuation diminishes invasion, migration, stem cell characteristics, and chemoresistance in human pancreatic cancer cells (42). Additionally, the authors showed correlation between EMT and increased SUV420H2 expression during the pathological progression of PDAC (42).…”

Section: Hnf4αmentioning

confidence: 94%

“…J Gastrointest Oncol 2018;9(6):1005-1013 jgo.amegroups.com in pancreatic cancer, demonstrating that the histone methyltransferase SUV420H2 acts as an orchestrator of epithelial/mesenchymal states (42). SUV420H2 induces silencing of key drivers of epithelial cell identity, such as HNF4α and FoxA1, and its attenuation diminishes invasion, migration, stem cell characteristics, and chemoresistance in human pancreatic cancer cells (42). Additionally, the authors showed correlation between EMT and increased SUV420H2 expression during the pathological progression of PDAC (42).…”

Section: Hnf4αmentioning

confidence: 99%

See 1 more Smart Citation

The role of lineage specifiers in pancreatic ductal adenocarcinoma

Camolotto¹,

Belova²,

Snyder³

2018

J. Gastrointest. Oncol

View full text Add to dashboard Cite

Over the last decade, multiple genomics studies have led to the identification of discrete molecular subtypes of pancreatic ductal adenocarcinoma. A general theme has emerged that most pancreatic ductal adenocarcinoma (PDAC) can be grouped into two major subtypes based on cancer cell autonomous properties: classical/pancreatic progenitor and basal-like/squamous. The classical/progenitor subtype expresses higher levels of lineage specifiers that regulate endodermal differentiation than the basal-like/ squamous subtype. The basal-like/squamous subtype confers a worse prognosis, raising the possibility that loss of these lineage specifiers might enhance the malignant potential of PDAC. Here, we discuss several of these differentially expressed lineage specifiers and examine the evidence that they might play a functional role in PDAC biology.

show abstract

Section: Hnf4αmentioning

confidence: 94%

Section: Hnf4αmentioning

confidence: 99%

The role of lineage specifiers in pancreatic ductal adenocarcinoma

Camolotto¹,

Belova²,

Snyder³

2018

J. Gastrointest. Oncol

View full text Add to dashboard Cite

show abstract

“…164,165 Meanwhile, KMT5C silences expression of the mesenchymal-to-epithelial transition (MET)promoting transcription factors FOXA1, OVOL1, and OVOL2 via its repressive mark H4K20me3 in PC. 166 Furthermore, PRMT1 can bind to the promoter region of CTNNB1 and increase the β-catenin protein level in PC cells, 167 but whether this effect is related to histone methylation needs further exploration.…”

Section: Emtmentioning

confidence: 99%

The role of histone methylation in the development of digestive cancers: a potential direction for cancer management

Chen

Ren

Yang

et al. 2020

Sig Transduct Target Ther

View full text Add to dashboard Cite

Digestive cancers are the leading cause of cancer-related death worldwide and have high risks of morbidity and mortality. Histone methylation, which is mediated mainly by lysine methyltransferases, lysine demethylases, and protein arginine methyltransferases, has emerged as an essential mechanism regulating pathological processes in digestive cancers. Under certain conditions, aberrant expression of these modifiers leads to abnormal histone methylation or demethylation in the corresponding cancer-related genes, which contributes to different processes and phenotypes, such as carcinogenesis, proliferation, metabolic reprogramming, epithelial-mesenchymal transition, invasion, and migration, during digestive cancer development. In this review, we focus on the association between histone methylation regulation and the development of digestive cancers, including gastric cancer, liver cancer, pancreatic cancer, and colorectal cancer, as well as on its clinical application prospects, aiming to provide a new perspective on the management of digestive cancers.

show abstract

“…Knockdown of SUV420H2 elicited MET on a molecular and functional level. An analysis of human pancreatic cancer biopsies suggests that high levels of SUV420H2 correlate with a loss of epithelial characteristics and progressively invasive cancer [86]. SET8 (also known as PR-Set7/9, SETD8, KMT5A), a member of the SET domain-containing methyltransferase family that specifically target H4K20 for monomethylation, physically interacts with TWIST to promote EMT and invasion by breast cancer cells [87].…”

Section: Transcriptional Repression and Lysine Methylationmentioning

confidence: 99%

The Landscape of Histone Modification in Cancer Metastasis

Qiu¹,

Wang²,

Wu³

2018

Cancer Metastasis

View full text Add to dashboard Cite

Metastasis represents one of the most devastating aspects of cancer. Epithelial to mesenchymal transition (EMT) has been shown to play a critical role in tumorigenic metastasis. During metastatic progression, both genetic and epigenetic modifications endow cancer cells with properties that modulate the capacity for metastatic success. Histone modification is profoundly altered in cancer cells and contributes to cancer metastasis by controlling different metastatic phenotypes. Here, we first review histone modifications and discuss their roles in EMT and metastasis, with a particular focus on histone methylation and acetylation. Second, we review the major histone modification enzymes that control chromatin in cancer metastasis. Third, we discuss the transcriptional regulation concerted by these enzymes with EMT transcription factors at different molecular layers. Finally, we discuss pharmacologic manipulation of histone modification enzymes for metastasis treatment. A comprehensive understanding of histone modification in metastasis will not only provide new insights into our knowledge of cancer progression and metastasis, but also offer a novel approach for the development of innovative therapeutic strategies.

show abstract

SUV420H2 is an epigenetic regulator of epithelial/mesenchymal states in pancreatic cancer

Cited by 37 publications

References 70 publications

The role of lineage specifiers in pancreatic ductal adenocarcinoma

The role of lineage specifiers in pancreatic ductal adenocarcinoma

The role of histone methylation in the development of digestive cancers: a potential direction for cancer management

The Landscape of Histone Modification in Cancer Metastasis

Contact Info

Product

Resources

About