Matrine Inhibits Disturbed Flow–Enhanced Migration via Downregulation of ERK1/2–MLCK Signaling Vascular Smooth Muscle Cells

Zhu, Ping; Chen, Jimei; Guo, Huiming; Fan, Xiaoping; Zhang, Xiao-Shen; Fan, Ruixin; Zheng, Shaoyi; Wu, Ruo-bin; Xiao, Xuejun; Huang, Huanlei; Zhu, Xiaolan; Liu, Huaipu; Long, Guang; Chen, Yanfang; Zhuang, Jian

doi:10.1016/j.avsg.2011.10.006

Cited by 6 publications

(5 citation statements)

References 15 publications

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“…Myosin Light Chain Kinase (MLCK, dependent increases in myosin ATPase activity), a key Ca 2+ / Calmodulin (CaM)-dmependent effector, is a myosin regulator in the lamella and contractile ring, and could regulate nonmuscle myosin II activity via phosphorylation of Ser19, Thr18 on myosin light chains (MLC) (Chew et al, 2002), and assemble in protrusive during cell migration (Kolega, 2003). It has been reported that the activation and increased expression of MLCK are crucial to trigger non-muscle cell and smooth muscle cell motility (Even-Ram et al, 2007;Sun et al, 2011;Zhu et al, 2012). MLCK in cancer cell migration remains controversial.…”

Section: Introductionmentioning

confidence: 99%

Melatonin inhibits the Migration of Colon Cancer RKO cells by Down-regulating Myosin Light Chain Kinase Expression through Cross-talk with p38 MAPK

Zou

Wei²,

Hu³

et al. 2015

Asian Pacific Journal of Cancer Prevention

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Background: Melatonin, which is mainly produced by the pineal gland, has a good inhibitory effect on cell growth of multiple cancer types. However, the underlying molecular mechanisms of anti-tumor activity for colon cancer have not been fully elucidated. In this study, we investigated the effects of melatonin on migration in human colon cancer RKO cells and the potential molecular mechanisms. Materials and Methods: The viability of RKO cells was investigated by MTT assay after treatment with melatonin, SB203580 (p38 inhibitor) and phorbol 12-myristate 13-acetate (PMA, MAPK activator) alone or in combination for 48h. The effects of melatonin, and ML-7, a selective inhibitor of myosin light chain kinase (MLCK), and SB203580, and PMA on the migration of RKO cells were analyzed by in vitro scratch-wound assay. The relative mRNA levels of MLCK was assessed by real-time quantitative RT-PCR. Western blotting analysis was performed to examine the expression of MLCK, phosphorylation of myosin light chain (pMLC) and p38 (pp38). Results: The proliferation and migration of human colon cancer RKO cells were inhibited significantly after treatment with melatonin. The expression levels of MLCK and phosphorylation of MLC of RKO cells were reduced, and real-time quantitative RT-PCR showed that melatonin had significant effects on suppressing the expression of MLCK. Furthermore, the phosphorylation level of p38, which showed the same trend, was also reduced when cells were treated by melatonin. In addition, ML-7 (25umol/l) could down-regulate the phosphorylation of p38. Conclusions: Melatonin could inhibit the proliferation and migration of RKO cells, and further experiments confirmed that p38 MAPK plays an important role in regulating melatonin-induced migration inhibition through down-regulating the expression and activity of MLCK.

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Section: Introductionmentioning

confidence: 99%

Melatonin inhibits the Migration of Colon Cancer RKO cells by Down-regulating Myosin Light Chain Kinase Expression through Cross-talk with p38 MAPK

Zou

Wei²,

Hu³

et al. 2015

Asian Pacific Journal of Cancer Prevention

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“…It has been reported that the rate of proliferation is inhibited in gastric cancer cells through induction of apoptosis via targeting the mitogen-activated protein kinase (MAPK) pathway ( 21 ). It was reported that ERK1/2 phosphorylation can be selectively inhibited either by its inhibitor (PD98059) or by using drugs, including matrine ( 22 ). The proliferation of cancer cells is regulated by one of the important members of the MAPK family, ERK 1/2 ( 23 ).…”

Section: Discussionmentioning

confidence: 99%

Fisetin inhibits the proliferation of gastric cancer cells and induces apoptosis through suppression of ERK 1/2 activation

et al. 2018

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The present study aimed to investigate the effect of fisetin on proliferation and apoptosis of gastric cancer cells, as well as the underlying mechanism. Proliferation in SGC7901 cancer and GES-1 normal cells was analyzed using a CCK-8 assay. Apoptosis was analyzed using an Annexin V/Propidium Iodide apoptosis kit and phosphorylation of extracellular signal-regulated kinase (ERK) 1/2 was analyzed by western blot assay. Treatment of SGC7901 cells with various concentrations (1, 5, 10, 15 and 20 µM) of fisetin for 48 h resulted in a concentration dependent reduction in proliferation. Flow cytometry revealed a marked increase in apoptosis from 5 µM concentration of fisetin after 48 h. The percentage of apoptotic cells increased to 87% following treatment with 15 µM fisetin for 48 h, compared with 2% in control. Treatment of SGC7901 cells with fisetin for 48 h resulted in a reduction in the activation of ERK 1/2 in a concentration-dependent manner. The reduction in activation of ERK 1/2 was significant following treatment with 15 µM fisetin for 48 h. The inhibitory effect of fisetin on activation of ERK 1/2 was further demonstrated using the ERK 1/2 inhibitor, PD98059. The results indicated a significant reduction in the proliferation of SGC7901 cells following treatment with PD98059 (P<0.002). The reduction by PD98059 administration was comparable to that observed following fisetin treatment for 48 h. In conclusion, the current study demonstrates that fisetin inhibits the proliferation of gastric cancer cells and induces apoptosis through suppression of ERK 1/2 activation. Thus, fisetin may have therapeutic applications in the treatment of gastric cancer.

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“…Next the phosphorylated MLC promotes myosin interacting with actin to drive cell moving on (Shin et al, 2009;Sun et al, 2011). Studies have shown that the phosphorylation of ERK1/2 promoted the activation of MLCK to trigger cell migration in smooth muscle cells, vascular endothelial cells, and breast cancer cells (Srinivas et al, 2004;Zhu et al, 2012b;2014a;Harrison et al, 2013). Besides, there exist other studies revealing the crosstalk between MLCK and ERK1/2 in the process of cell migration (Zhou et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

“…In our previous studies, it was explored that ATPR might inhibit tumor cells migration by down-regulating the expression of MLCK involving p38 signaling pathway (Wang et al, 2013a), one of MAPKs pathway cascade. The mitogen-activated protein kinases (MAPKs) cascades include three classical signal pathways: p38, ERK1/2 and JNK, which play crucial roles in different physiological processes, such as cell growth, apoptosis and inflammatory reaction (Zhu et al, 2012b;2014a;Wang et al, 2013c). It was also reported that the elevation of ERK1/2 might activate the MLCK along with a series of downstream pathways activation (Srinivas et al, 2004;Zhou et al, 2008;Muralidharan-Chari et al, 2009;Zhu et al, 2012b;2014a;Harrison et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

“…The myosin light chain kinase (MLCK ) is one kind of protein kinases which is Ca 2+ /Calmodulin-dependent (Zhou et al, 2008). The activation and increased expression of MLCK are crucial to trigger smooth muscle cell and non-muscle cell motility (Sun et al, 2011;Zhu et al, 2012b). Some researches have reported that the overexpression of MLCK was occurred in many cancer cells (Kucharczak et al, 2001;Mills et al, 2011;Wang et al, 2013d).…”

Section: Introductionmentioning

confidence: 99%

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A Novel All-trans Retinoid Acid Derivative N-(3-trifluoromethyl-phenyl)-Retinamide Inhibits Lung Adenocarcinoma A549 Cell Migration through Down-regulating Expression of Myosin Light Chain Kinase

Fan

Cheng²,

Wang³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Matrine Inhibits Disturbed Flow–Enhanced Migration via Downregulation of ERK1/2–MLCK Signaling Vascular Smooth Muscle Cells

Cited by 6 publications

References 15 publications

Melatonin inhibits the Migration of Colon Cancer RKO cells by Down-regulating Myosin Light Chain Kinase Expression through Cross-talk with p38 MAPK

Melatonin inhibits the Migration of Colon Cancer RKO cells by Down-regulating Myosin Light Chain Kinase Expression through Cross-talk with p38 MAPK

Fisetin inhibits the proliferation of gastric cancer cells and induces apoptosis through suppression of ERK 1/2 activation

A Novel All-trans Retinoid Acid Derivative N-(3-trifluoromethyl-phenyl)-Retinamide Inhibits Lung Adenocarcinoma A549 Cell Migration through Down-regulating Expression of Myosin Light Chain Kinase

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