Activation of AKT negatively regulates the pro-apoptotic function of death-associated protein kinase 3 (DAPK3) in prostate cancer

Das, Trinath P.; Suman, Suman; John, Axel; Pal, Devendra; Edwards, Angelena; Alatassi, Houda; Ankem, Murali K.; Damodaran, Chendil

doi:10.1016/j.canlet.2016.04.028

Cited by 27 publications

(26 citation statements)

References 38 publications

(51 reference statements)

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“…We observed a trend for insulin-induced DAPK3 methylation in primary human skeletal muscle that persisted over 4 h Although not statistically significant, this effect mirrored the insulin-induced DNA methylation of DAPK3 in incubated human muscle strips. Interestingly, DAPK3 is a tumor suppressor that is frequently methylated or mutated in many cancer types (36) and is negatively regulated by Akt signaling (37). DAPK3 is important for myosin light chain phosphorylation, leading to muscle contraction or cell mobility (34).…”

Section: Discussionmentioning

confidence: 99%

Insulin and Glucose Alter Death-Associated Protein Kinase 3 (DAPK3) DNA Methylation in Human Skeletal Muscle

et al. 2016

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DNA methylation is altered by environmental factors. We hypothesized that DNA methylation is altered in skeletal muscle in response to either insulin or glucose exposure. We performed a genome-wide DNA methylation analysis in muscle from healthy men before and after insulin exposure. DNA methylation of selected genes was determined in muscle from healthy men and men with type 2 diabetes before and after a glucose tolerance test. Insulin altered DNA methylation in the 3' untranslated region of the calcium pump gene. Insulin increased DNA methylation in the gene body of, a gene involved in cell proliferation, apoptosis, and autophagy. methylation was reduced in patients with type 2 diabetes. Carbohydrate ingestion reduced DNA methylation in healthy men and men with type 2 diabetes, suggesting glucose may play a role. Supporting this, DNA methylation was inversely correlated with the 2-h glucose concentration. Whereas glucose incorporation to glycogen was unaltered by small interfering RNA against, palmitate oxidation was increased. In conclusion, insulin and glucose exposure acutely alter the DNA methylation profile of skeletal muscle, indicating that DNA methylation constitutes a rapidly adaptive epigenetic mark. Furthermore, insulin and glucose modulate DNA methylation in a reciprocal manner, suggesting a feedback loop in the control of the epigenome.

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Section: Discussionmentioning

confidence: 99%

Insulin and Glucose Alter Death-Associated Protein Kinase 3 (DAPK3) DNA Methylation in Human Skeletal Muscle

et al. 2016

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“…Recently, the oncogenic role of DAPK3 in the A549 NSCLC cell line was explored. DAPK3 was found essential for the proliferation, migration, invasion, and colony formation in A549 cell line in vitro and in vivo, suggesting DAPK3 as a novel target for treatment of NSCLC . DAPK3 knockout in A549 cells showed G 1 /G 0 cell cycle arrest.…”

Section: Dapks Cellular Functionsmentioning

confidence: 96%

Death‐associated protein kinase (DAPK) family modulators: Current and future therapeutic outcomes

Farag

Roh

2018

Medicinal Research Reviews

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Serine/threonine kinases (STKs) represent the majority of discovered kinases to date even though a few Food and Drug Administration approved STKs inhibitors are reported. The third millennium came with the discovery of an important group of STKs that reshaped our understanding of several biological signaling pathways. This family was named death-associated protein kinase family (DAPK family). DAPKs comprise five members (DAPK1, DAPK2, DAPK3, DRAK1, and DRAK2) and belong to the calcium/calmodulin-dependent kinases domain. As time goes on, the list of biological functions of this family is constantly updated. The most extensively studied member is DAPK1 (based on the publications number and Protein Data Bank reported crystal structures) that plays fundamental biological roles depending on the cellular context. DAPK1 regulates apoptosis, autophagy, contributes to the pathogenesis of Alzheimer's disease, acts as a tumor suppressor, inhibits metastasis, mediates the body responses to viral infections, and regulates the synaptic plasticity and depression. For their biological roles, several DAPKs' modulators have been reported for treatment of many diseases as well as acting as probe compounds to facilitate the understanding of the biological functions elicited by this family. Despite that, the number of reported modulators is still limited and more research needs to be conducted on the discovery of novel strategies to activate or inhibit this family. In this report, we aim at drawing more attention to this family by reviewing the recent updates regarding the structure, biological roles, and regulation of this family. In addition, the small-molecule modulators of this family are reviewed in details with their potential therapeutic outcomes evaluated to help medicinal chemists develop more potent and selective possible drug candidates.

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“…The Dapk family are actin cytoskeleton‐associated Ca2 + /calmodulin (CaM)‐regulated serine/threonine kinases reported to regulate cell death via various mechanisms including interferon‐γ, c‐Myc, and anoikis . Dapk3 has been shown to exert apoptotic function through mitochondrial pathways and to have tumor‐suppressing qualities .…”

Section: Resultsmentioning

confidence: 99%

Tropomyosin isoforms have specific effects on the transcriptome of undifferentiated and differentiated B35 neuroblastoma cells

et al. 2018

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Tropomyosins, a family of actin‐associated proteins, bestow actin filaments with distinct biochemical and physical properties which are important for determining cell shape and regulating many cellular processes in eukaryotic cells. Here, we used RNA‐seq to investigate the effect of four tropomyosin isoforms on gene expression in undifferentiated and differentiated rat B35 neuroblastoma cells. In undifferentiated cells, overexpression of tropomyosin isoforms Tpm1.12, Tpm2.1, Tpm3.1, and Tpm4.2 differentially regulates a vast number of genes, clustering into several gene ontology terms. In differentiated cells, tropomyosin overexpression exerts a much weaker influence on overall gene expression. Our findings are particularly compelling because they demonstrate that tropomyosin‐dependent changes are attenuated once the cells are induced to follow a defined path of differentiation. Database Sequence data for public availability are deposited in the European Nucleotide Archive under the accession number PRJEB24136.

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Activation of AKT negatively regulates the pro-apoptotic function of death-associated protein kinase 3 (DAPK3) in prostate cancer

Cited by 27 publications

References 38 publications

Insulin and Glucose Alter Death-Associated Protein Kinase 3 (DAPK3) DNA Methylation in Human Skeletal Muscle

Insulin and Glucose Alter Death-Associated Protein Kinase 3 (DAPK3) DNA Methylation in Human Skeletal Muscle

Death‐associated protein kinase (DAPK) family modulators: Current and future therapeutic outcomes

Tropomyosin isoforms have specific effects on the transcriptome of undifferentiated and differentiated B35 neuroblastoma cells

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