Overexpression of SET and MYND domain-containing protein 2 (<i>SMYD2</i>) is associated with poor prognosis in pediatric B lineage acute lymphoblastic leukemia

Zhang, Ping; Ruan, JinFei; Weng, W W; Tang, Yongmin

doi:10.1080/10428194.2019.1675875

Cited by 9 publications

(3 citation statements)

References 23 publications

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“…Similar results were obtained by Zhang et al. who observed overexpression of SMYD2 in the bone marrow of children with B lineage acute lymphoblastic leukaemia, which was associated with bad prognosis (including increased white blood cell count and less overall survival and tumour-free survival) and a reduction of SMYD2 expression levels after remission ( Zhang et al., 2020 ). Animal studies demonstrated that, although germ-line SMYD2 KO mice are viable, healthy and display normal haematopoiesis, SMYD2 deficiency delayed and reduced penetrance of death due to MLL-AF9/NRas G12D -induced acute myeloid leukaemia.…”

Section: Blood Cell Cancerssupporting

confidence: 85%

The SMYD family proteins in immunology: An update of their obvious and non-obvious relations with the immune system

Rubio-Tomás

2021

Heliyon

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Epigenetics is an emerging field, due to its relevance in the regulation of a wide range of biological processes. The Su(Var)3–9, Enhancer-of-zeste and Trithorax (SET) and Myeloid, Nervy, and DEAF-1 (MYND) domain-containing (SMYD) proteins, named SMYD1, SMYD2, SMYD3, SMYD4 and SMYD5, are enzymes that catalyse methylation of histone and non-histone substrates, thereby playing a key role in gene expression regulation in many biological contexts, such as muscle development and physiology, haematopoiesis and many types of cancer. This review focuses on a relatively unexplored aspect of SMYD family members - their relation with immunology. Here, immunology is defined in the broadest sense of the word, including basic research on macrophage function or host immunity against pathogen infection, as well as clinical studies, most of which are centred on blood cancers.

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Section: Blood Cell Cancerssupporting

confidence: 85%

The SMYD family proteins in immunology: An update of their obvious and non-obvious relations with the immune system

Rubio-Tomás

2021

Heliyon

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“…A decrease in SMYD2 expression was observed 29 days after chemotherapy in most of the patients who responded to the treatment (leukaemia remission was determined by the presence of less than 5% of leukaemic cells in bone marrow) (Sakamoto et al 2014). Similar results were obtained by Zhanget al who observed overexpression of SMYD2 in the bone marrow of children with B lineage acute lymphoblastic leukaemia, which was associated with bad prognosis (including increased white blood cell count and less overall survival and tumour-free survival) and a reduction of SMYD2 expression levels after remission (Zhang et al 2020). Animal studies demonstrated that, although germ-line SMYD2 KO mice are viable, healthy and display normal haematopoiesis, SMYD2 deficiency delayed and reduced penetrance of death due to MLL-AF9/NRas G12Dinduced acute myeloid leukaemia.…”

Section: Smyd2supporting

confidence: 76%

The SMYD family proteins in immunology

Rubio-Tomás

2021

Preprint

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Epigenetics is an emerging field, due to its relevance in the regulation of a wide range of biological processes. The Su(Var)3-9, Enhancer-of-zeste and Trithorax (SET) and Myeloid, Nervy, and DEAF-1 (MYND) domain-containing (SMYD) proteins, named SMYD1, SMYD2, SMYD3, SMYD4 and SMYD5, are enzymes that catalyse methylation of histone and non-histone substrates, thereby playing a key role in gene expression regulation in many biological contexts, such as muscle development and physiology, haematopoiesis and many types of cancer. This review focuses on a relatively unexplored aspect of SMYD family members - their relation with immunology. Here, immunology is defined in the broadest sense of the word, including basic research on macrophage function or host immunity against pathogen infection, as well as clinical studies, most of which are centred on blood cancers.

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“…These pathways include the critical signaling cascade RTK/Ras, the downstream signaling cascades of the RTK/Ras pathway, such as the mitogen-activated protein kinase (MAPK) pathway, and the PI3K/AKT pathway[ 16 , 27 , 28 , 30 , 31 ]. As dysregulation of these signaling pathways is an almost universal phenomenon in cancer, it is not surprising that SMYD2 overexpression has been linked with tumor development and progression in multiple human cancers, such as gastric cancer[ 33 ], esophageal squamous cell carcinoma[ 34 ], breast cancer[ 30 ], bladder cancer[ 23 ], colon cancer[ 31 , 35 ], colorectal cancer[ 36 ], hepatocellular carcinoma[ 14 ], acute lymphoblastic leukemia[ 37 , 38 ], hematopoietic leukemias[ 39 ], head and neck squamous cell carcinoma[ 15 ], lung adenocarcinoma[ 13 ], papillary thyroid carcinoma[ 40 ], cervical cancer[ 41 , 42 ], ovarian clear cell carcinoma[ 43 , 44 ], and renal cell carcinoma[ 45 , 46 ] (Table 2 ).…”

Section: Introductionmentioning

confidence: 99%

Mechanistic and functional extrapolation of SET and MYND domain-containing protein 2 to pancreatic cancer

Alshammari¹,

Zhang²,

Yang³

2022

WJG

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Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal neoplasms worldwide and represents the vast majority of pancreatic cancer cases. Understanding the molecular pathogenesis and the underlying mechanisms involved in the initiation, maintenance, and progression of PDAC is an urgent need, which may lead to the development of novel therapeutic strategies against this deadly cancer. Here, we review the role of SET and MYND domain-containing protein 2 (SMYD2) in initiating and maintaining PDAC development through methylating multiple tumor suppressors and oncogenic proteins. Given the broad substrate specificity of SMYD2 and its involvement in diverse oncogenic signaling pathways in many other cancers, the mechanistic extrapolation of SMYD2 from these cancers to PDAC may allow for developing new hypotheses about the mechanisms driving PDAC tumor growth and metastasis, supporting a proposition that targeting SMYD2 could be a powerful strategy for the prevention and treatment of PDAC.

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Overexpression of SET and MYND domain-containing protein 2 (SMYD2) is associated with poor prognosis in pediatric B lineage acute lymphoblastic leukemia

Cited by 9 publications

References 23 publications

The SMYD family proteins in immunology: An update of their obvious and non-obvious relations with the immune system

The SMYD family proteins in immunology: An update of their obvious and non-obvious relations with the immune system

The SMYD family proteins in immunology

Mechanistic and functional extrapolation of SET and MYND domain-containing protein 2 to pancreatic cancer

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