Myosin light chain kinase MYLK1: Anatomy, interactions, functions, and regulation

Khapchaev, Asker Y.; Shirinsky, Vladimir P.

doi:10.1134/s000629791613006x

Cited by 44 publications

(25 citation statements)

References 184 publications

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“…Myosin light chain kinase (MYLK) regulates myosin activity through phosphorylation and dephosphorylation of the myosin light chain. Therefore, it is involved in many physiological processes, such as cell adhesion, cell proliferation, cell migration and infiltration (44). MYLK can increase the expression of epidermal growth factor receptor and activate the ERK/JNK signal pathway, which can ablate the adhesion between cells and increase the aggressiveness of breast cancer cells (45).…”

Section: Discussionmentioning

confidence: 99%

Bioinformatic screening and identification of downregulated hub genes in adrenocortical carcinoma

Zhang

Miao

et al. 2020

Exp Ther Med

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The molecular mechanisms of adrenocortical carcinoma (ACC) carcinogenesis and progression remain unclear. In the present study, three microarray datasets from the Gene Expression Omnibus database were screened, which identified a total of 96 differentially expressed genes (DEGs). A protein-protein interaction network (PPI) was established for these DEGs and module analysis was performed using STRING and Cytoscape. A total of eight hub genes were identified from the most significant module; namely, calponin 1 (CNN1), myosin light chain kinase (MYLK), cysteine and glycine rich protein 1 (CSRP1), myosin heavy chain 11 (MYH11), fibulin extracellular matrix protein 2 (EFEMP2), fibulin 1 (FBLN1), microfibril associated protein 4 (MFAP4) and fibulin 5 (FBLN5). The biological functions of these hub genes were analyzed using the DAVID online tool. Changes in the expression of hub genes did not affect overall survival; however, downregulated EFEMP2 decreased disease-free survival. CSRP1 and MFAP4 expression levels were associated with adverse clinicopathological features. In conclusion, although all eight hub genes were downregulated in ACC, they appeared to have important functions in ACC carcinogenesis and progression. Identification of these genes complements the genetic expression profile of ACC and provides insight for the diagnosis, treatment and prognosis of ACC.

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Section: Discussionmentioning

confidence: 99%

Bioinformatic screening and identification of downregulated hub genes in adrenocortical carcinoma

Zhang

Miao

et al. 2020

Exp Ther Med

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“…Aside from melanoma, AP-1/TEAD modulates the expression of a core set of genes involved in the migration and invasion of different types of cancer cells, including neuroblastoma, colorectal or lung cancer 42 . Regarding the AP-1 transcriptional targets it is worth noting that melanoma cells failing to die up-regulate several genes such as PTX3 , MYLK , SPP1 or RAC2 , all shown to be regulated by AP-1 and involved in metastasis 43 44 45 46 . While in these studies the AP-1/c-JUN transcription factors are activated by a plethora of stimuli such as cytokines, growth factors, UV irradiation or activating mutations in N-RAS and B-RAF genes, in our case, JNK activation was most probably induced as a consequence of minority MOMP 7 .…”

Section: Discussionmentioning

confidence: 99%

Failed apoptosis enhances melanoma cancer cells aggressiveness

Berthenet

Ferrer

Popgeorgiev

et al. 2019

Preprint

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Triggering apoptosis remains an efficient strategy to treat cancer. However, apoptosis is no longer a final destination, since cells can undergo partial apoptosis without dying. Recent evidence shows that partial mitochondrial permeabilization and non-lethal caspase activation occur under certain circumstances, though it remains unclear how failed apoptosis impacts established cancers. Using a cancer cell model to trigger non-lethal caspase activation based on either BH3-only protein expression or chemotherapy treatment, we found that melanoma cancer cells failing to undergo complete apoptosis have a particular transcriptomic signature associated with focal adhesions, transendothelial migration and modifications of actin cytoskeleton.In line with this, cancer cells surviving apoptosis have a gain in migratory and invasive properties both in vitro (random migration, chemotaxis, wound healing and invasion assays) and in vivo (in a model of zebrafish metastasis)We further demonstrate that the failed apoptosis-associated gain in invasiveness is regulated by the c-Jun N-terminal kinase (JNK) pathway while its RNA seq signature is found in metastatic melanoma. These findings are highly significant for understanding how cell death can both cure and promote cancer.3

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“…The mylk-1 gene encodes a 220 kDa MLCK, a 130 kDa MLCK and telokin, and is widely expressed in a diverse range of tissues and cells (18,19). MLCK is involved in adhesion and migration, which are basic characteristics of cells (20,21). A previous pharmacological study revealed that the inhibition of MLCK changed cell motility and wound contraction (22).…”

Section: Discussionmentioning

confidence: 99%

Effects of β‑hydroxybutyric acid and ghrelin on the motility and inflammation of gastric antral smooth muscle cells involving the regulation of growth hormone secretagogue receptor

et al. 2019

Mol Med Report

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Ghrelin is an orexigenic hormone that is produced by gastric cells. Ghrelin stimulates food intake and increases gastric movement. In rat model, injected β-hydroxybutyric acid (β-HB) leads to a decrease in body weight. It has been reported that patients with gastric erosions are slower to evacuate the stomach. The aim of the present study was to investigate the effects of ghrelin and β-HB on motility and inflammation in rat gastric antral smooth muscle cells (GASMCs). GASMCs were extracted from rat gastric antrum. Cell viability was determined using the Cell Counting Kit-8 assay. A reactive oxygen species (ROS) assay kit was used to analyze the levels of ROS using flow cytometry. Protein levels were determined using western blotting, and the expression levels of mRNAs were evaluated using reverse transcription-quantitative PCR. β-HB inhibited the expression of myosin regulatory light polypeptide 9 (MYL9), myosin light chain kinase (MLCK), transforming protein RhoA (RhoA), Rho-associated protein kinase-1 (ROCK-1) and growth hormone secretagogue receptor (GHS-R). By contrast, ghrelin increased the expression of MYL9, MLCK, RhoA, ROCK-1 and GHS-R in β-HB-treated GASMCs. β-HB increased the levels of tumor necrosis factor (TNF)-α, interleukin (IL)-6 and ROS, and decreased the levels of manganese (Mn) superoxide dismutase (SOD), copper/zinc (Cu/Zn)SOD and catalase. Ghrelin decreased the expression of TNF-α, IL-6, ROS and catalase, whereas ghrelin promoted the expression of MnSOD and Cu/ZnSOD in β-HB-treated GASMCs. Short interfering RNA targeting GHS-R inhibited the expression of MYL9, MLCK, RhoA and ROCK-1, and increased the levels of TNF-α, IL-6 and ROS in β-HB-treated or ghrelin-treated GASMCs. The present study provided preliminary evidence that β-HB inhibits the motility of GASMCs and promotes inflammation in GASMCs, whereas ghrelin decreases these effects. GHS-R acted as a primary regulator of motility and inflammation in GASMCs treated with β-HB and ghrelin.

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Myosin light chain kinase MYLK1: Anatomy, interactions, functions, and regulation

Cited by 44 publications

References 184 publications

Bioinformatic screening and identification of downregulated hub genes in adrenocortical carcinoma

Bioinformatic screening and identification of downregulated hub genes in adrenocortical carcinoma

Failed apoptosis enhances melanoma cancer cells aggressiveness

Effects of β‑hydroxybutyric acid and ghrelin on the motility and inflammation of gastric antral smooth muscle cells involving the regulation of growth hormone secretagogue receptor

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