The NSD3L histone methyltransferase regulates cell cycle and cell invasion in breast cancer cells

Zhou, Zhangle; Thomsen, Rie; Kahns, Søren; Nielsen, Anders Lade

doi:10.1016/j.bbrc.2010.06.119

Cited by 37 publications

(36 citation statements)

References 16 publications

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“…Moreover, NSD3 is amplified in breast cancer cell lines and primary breast carcinomas (37, 38). NSD3 has been reported to contribute to the transformed phenotype and invasiveness of these breast cancer cells (39, 40). Most recently, mutations in NSD3 have been identified in pancreatic adenocarcinoma (41).…”

Section: Discussionmentioning

confidence: 99%

NSD3–NUT Fusion Oncoprotein in NUT Midline Carcinoma: Implications for a Novel Oncogenic Mechanism

et al. 2014

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NUT midline carcinoma (NMC) is an aggressive subtype of squamous cell carcinoma that typically harbors BRD4/3-NUT fusion oncoproteins that block differentiation and maintain tumor growth. In 20% of cases NUT is fused to uncharacterized non-BRD gene(s). We established a new patient-derived NMC cell line (1221) and demonstrated that it harbors a novel NSD3-NUT fusion oncogene. We find that NSD3-NUT is both necessary and sufficient for the blockade of differentiation and maintenance of proliferation in NMC cells. NSD3-NUT binds to BRD4, and BRD bromodomain inhibitors induce differentiation and arrest proliferation of 1221 cells. We find further that NSD3 is required for the blockade of differentiation in BRD4-NUT-expressing NMCs. These findings identify NSD3 as a novel critical oncogenic component and potential therapeutic target in NMC.

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Section: Discussionmentioning

confidence: 99%

NSD3–NUT Fusion Oncoprotein in NUT Midline Carcinoma: Implications for a Novel Oncogenic Mechanism

et al. 2014

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“…By contrast, knockdown of NSD3 reduced proliferation and promoted cell death in 8p11–12-amplified breast cancer cells and significantly decreased anchorage-dependent and anchorage-independent growth of pancreatic adenocarcinoma and small-cell lung cancer-derived cell lines (Yang et al 2010; Mahmood et al 2013). In addition, knockdown of NSD3 expression induced G 2 /M cell cycle arrest and suppressed proliferation of breast, bladder and lung cancer cell lines (Zhou et al 2010; Kang et al 2013). Expression profile analysis demonstrated that NSD3 affected the expression of a number of genes known to play crucial roles in cell cycle progression (Kang et al 2013).…”

Section: Nsd3 Role In Cancermentioning

confidence: 99%

The Role of Nuclear Receptor–Binding SET Domain Family Histone Lysine Methyltransferases in Cancer

Bennett

Swaroop

Troche

et al. 2017

Cold Spring Harb Perspect Med

142

184

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The Nuclear receptor-binding SET Domain (NSD) family of histone H3 lysine 36 methyl transferases is comprised of NSD1, NSD2 (MMSET/WHSC1), and NSD3 (WHSC1L1). These enzymes recognize and catalyze methylation of histone lysine marks to regulate chromatin integrity and gene expression. The growing number of reports demonstrating that alterations or translocations of these genes fundamentally affect cell growth and differentiation leading to developmental defects illustrates the importance of this family. In addition, overexpression, gain of function somatic mutations and translocations of NSDs are associated with human cancer and can trigger cellular transformation in model systems. Here we review the functions of NSD family members and the accumulating evidence that these proteins play key roles in tumorigenesis. Since epigenetic therapy is an important emerging anti-cancer strategy, understanding the function of NSD family members may lead to the development of novel therapies.

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“…NSD3 has also been found amplified in breast cancer, pancreatic cancer and lung squamous cell carcinoma, and siRNA based functional data in breast cancer support a critical role of NSD3 in tumorigenesis, growth, survival and invasion (Angrand et al, 2001;Garcia et al, 2005;Tonon et al, 2005;Yang et al, 2010;Zhou et al, 2010).In addition to NSD3, the KMTs SETDB1, ASH1L, SMYD2 and SMYD3 undego amplification in over 10% of breast cancers, although functional data is not (yet) available (Liu et al, 2015).…”

Section: The H3k36 Methyltransferases Nsd1 2 and 3-an Example For Gmentioning

confidence: 91%

Histone profiles in cancer

Riedel

Neff

Bernt

2015

Pharmacology & Therapeutics

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The NSD3L histone methyltransferase regulates cell cycle and cell invasion in breast cancer cells

Cited by 37 publications

References 16 publications

NSD3–NUT Fusion Oncoprotein in NUT Midline Carcinoma: Implications for a Novel Oncogenic Mechanism

NSD3–NUT Fusion Oncoprotein in NUT Midline Carcinoma: Implications for a Novel Oncogenic Mechanism

The Role of Nuclear Receptor–Binding SET Domain Family Histone Lysine Methyltransferases in Cancer

Histone profiles in cancer

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