Activation of Mitogen-Activated Protein Kinases by Tributyltin in CCRF-CEM Cells: Role of Intracellular Ca2+

Yu, Zheng; Matsuoka, Masato; Wispriyono, Bambang; Iryo, Yoshihisa; Ichikawa, Hideki

doi:10.1006/taap.2000.9033

Cited by 52 publications

(31 citation statements)

References 31 publications

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“…It is also known that p38 MAPK can be activated during different types of chemotherapy. Genotoxic drugs like cisplatin (Losa et al, 2003) as well as kinase inhibitors or ultraviolet and g-irradiation (Brancho et al, 2003;Losa et al, 2003) are recognized as agents able to stimulate p38 MAPK as well as JNK pathways (Bulavin et al, 1999;Sanchez-Prieto et al, 2000;Yu et al, 2000). It was reported that stimulation of p38 MAPK and JNK activity is crucial for cisplatin-induced apoptosis (Benhar et al, 2001), but specific inhibition of JNK or p38 MAPK suppresses the drug-induced cell death process (Tibbles and Woodgett, 1999).…”

Section: Discussionmentioning

confidence: 99%

Indirubin-3′-monoxime inhibits autophosphorylation of FGFR1 and stimulates ERK1/2 activity via p38 MAPK

et al. 2007

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Indirubin-3 0 -monoxime is a derivative of the bis-indole alkaloid indirubin, an active ingredient of a traditional Chinese medical preparation that exhibits anti-inflammatory and anti-leukemic activities. Indirubin-3 0 -monoxime is mainly recognized as an inhibitor of cyclin-dependent kinases (CDKs) and glycogen synthase kinase-3. It inhibits proliferation of cultured cells, mainly through arresting the cells in the G1/S or G2/M phase of the cell cycle. Here, we report that indirubin-3 0 -monoxime is able to inhibit proliferation of NIH/3T3 cells by specifically inhibiting autophosphorylation of fibroblast growth factor receptor 1 (FGFR1), blocking in this way the receptormediated cell signaling. Indirubin-3 0 -monoxime inhibits the activity of FGFR1 at a concentration lower than that required for inhibition of phosphorylation of CDK2 and retinoblastoma protein and cell proliferation stimulated by fetal calf serum. The ability of indirubin-3 0 -monoxime to inhibit FGFR1 signaling was similar to that of the FGFR1 inhibitor SU5402. In addition, we found that indirubin-3 0 -monoxime activates long-term p38 mitogen-activated protein kinase activity, which stimulates extracellular signal-regulated kinase 1/2 in a way unrelated to the activity of FGFR1. Furthermore, we show that indirubin-3 0 -monoxime can inhibit proliferation of the myeloid leukemia cell line KG-1a through inhibition of the activity of the FGFR1 tyrosine kinase. The data presented here demonstrate previously unknown activities of indirubin-3 0 -monoxime that may have clinical implications.

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Section: Discussionmentioning

confidence: 99%

Indirubin-3′-monoxime inhibits autophosphorylation of FGFR1 and stimulates ERK1/2 activity via p38 MAPK

et al. 2007

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“…Among the triorganotin compounds, tributyltin induced the most marked phosphorylation of all of ERK, JNK and p38 MAPK 74) . While triphenyltin increased the levels of phosphorylated ERK and p38 MAPK slightly, trimethyltin and triethyltin did not induce the phosphorylation of MAPKs.…”

Section: ) Comparison Of Effects Of Organotins On Mapks Phosphorylationmentioning

confidence: 97%

“…When compared to TBTCl, a less marked phosphorylation of ERK, JNK and p38 MAPK was found in CCRF-CEM cells exposed to the same concentration (1 μM) of dibutyltin dichloride (DBTCl 2 ) or monobutyltin trichloride (MBTCl 3 ) for 1 hr 74) . The incubation with DBTCl 2 only slightly increased the levels of phosphorylated ERK and p38 MAPK, and MBTCl 3 exposure increased none of the MAPKs clearly.…”

Section: ) Comparison Of Effects Of Organotins On Mapks Phosphorylationmentioning

confidence: 99%

“…Since tributyltin, one of the environmental toxicants 71) , has been reported to cause apoptosis in leukemia T cell lines 72,73) , the phosphorylation status of MAPKs was examined in CCRF-CEM cells treated with tributyltin chloride (TBTCl) 74) . Incubation with 0.25-2.0 μM TBTCl for 1 hr induced a marked phosphorylation of ERK, JNK and p38 MAPK in a dose-dependent manner.…”

Section: ) Activation Of Mapks In Ccrf-cem Cellsmentioning

confidence: 99%

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Effects of Heavy Metals on Mitogen-Activated Protein Kinase Pathways.

Matsuoka

Ichikawa

2002

Environ. Health Prev. Med.

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The signaling pathways leading to cellular protection or cell death following exposure to heavy metals have not been fully clarified. Mitogen-activated protein kinases (MAPKs), i.e., extracellular signalregulated protein kinase (ERK), c-Jun NH 2 -terminal kinase (JNK) and p38 MAPK transmit extracellular signals into the nucleus, and have been shown to participate in a diverse array of cellular functions such as cell growth, differentiation and apoptosis. Treatment with cadmium, inorganic mercury or tributyltin can activate ERK, JNK and p38 MAPK, and induces the expression of c-fos and c-jun genes prior to the development of apoptosis. However, the members of the MAPK family appear to be differentially activated depending on the heavy metal and the cell type exposed. Consequently, various cellular responses may be caused by the distinct pattern of MAPKs activation. MAPKs may be one of the important cellular signal transduction pathways affected by various environmental pollutants, including heavy metals.

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“…In menschlichen NK-Zellen übte Tri-n-butylzinn dagegen keinen Einfluss auf die Apoptose aus, wie Untersuchungen zu den pro-apoptotischen Proteinen Bax und p53 sowie zu dem anti-apoptotischen Protein Bcl-2 zeigten (Aluoch et al 2007). Verschiedene Signalübertragungswege wurden aufgrund der durch Tri-n-butylzinn hervorgerufenen Mobilisierung von intrazellulärem, freiem Calcium und der daraus resultierenden Phosphorylierung von Mitogen-aktivierten Proteinkinasen beeinflusst: die MAP-Kinase JNK in PC12-Zellen (Nakatsu et al 2007), die MAP-Kinasen p38, JNK und ERK in menschlichen T-Zellen (Yu et al 2000) sowie die Proteinkinasen p38 und p44/42 in menschlichen NK-Zellen (Aluoch und Whalen 2005). Der durch Tri-n-butylzinn induzierte Verlust der Fähigkeit der NK-Zellen zur Bindung an Tumorzellen wurde durch einen Verlust der Oberflächen-Antigene CD16 und CD56 sowie durch die Verringerung der Expression der zytotoxisch wirksamen Proteine Granzyme B und Perforin (Thomas et al 2004) hervorgerufen.…”

Section: Störung Der Ca 2+ -Homöostaseunclassified

n‐Butylzinnverbindungen [MAK Value Documentation in German language, 2008]

2012

The MAK‐Collection for Occupational Health and Safety

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Veröffentlicht in der Reihe Gesundheitsschädliche Arbeitsstoffe , 44. Lieferung, Ausgabe 2008 Der Artikel enthält folgende Kapitel: Allgemeiner Wirkungscharakter Wirkungsmechanismus Toxikokinetik und Metabolismus Aufnahme, Verteilung, Ausscheidung Metabolismus Erfahrungen beim Menschen Einmalige Exposition Wiederholte Exposition Wirkung auf Haut und Schleimhäute Allergene Wirkung Tierexperimentelle Befunde und In‐vitro‐Untersuchungen Akute Toxizität Subakute, subchronische und chronische Toxizität Wirkung auf Haut und Schleimhäute Auge Allergene Wirkung Reproduktionstoxizität Genotoxizität Kanzerogenität Sonstige Wirkungen Bewertung

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Activation of Mitogen-Activated Protein Kinases by Tributyltin in CCRF-CEM Cells: Role of Intracellular Ca2+

Cited by 52 publications

References 31 publications

Indirubin-3′-monoxime inhibits autophosphorylation of FGFR1 and stimulates ERK1/2 activity via p38 MAPK

Indirubin-3′-monoxime inhibits autophosphorylation of FGFR1 and stimulates ERK1/2 activity via p38 MAPK

Effects of Heavy Metals on Mitogen-Activated Protein Kinase Pathways.

n‐Butylzinnverbindungen [MAK Value Documentation in German language, 2008]

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