Compounds > 5-5--6-6--tetrachloro-1-1--3-3--tetraethylbenzimidazolocarbocyanine

5-5--6-6--tetrachloro-1-1--3-3--tetraethylbenzimidazolocarbocyanine and Melanoma

5-5--6-6--tetrachloro-1-1--3-3--tetraethylbenzimidazolocarbocyanine has been researched along with Melanoma* in 1 studies

Other Studies

1 other study(ies) available for 5-5--6-6--tetrachloro-1-1--3-3--tetraethylbenzimidazolocarbocyanine and Melanoma

Article	Year
Activation of Jun N-terminal kinase is a mediator of vincristine-induced apoptosis of melanoma cells. Anti-cancer drugs, 2008, Volume: 19, Issue:2 The molecular changes involved in the induction of apoptosis by vincristine in melanoma have not yet been well defined. Two human melanoma cell lines showing moderate (Mel-RM) and high (IgR3) sensitivity to vincristine were selected from a panel of eight melanoma lines for analysis. Induction of apoptosis was caspase dependent, and was associated with increases in mitochondrial membrane permeability. Vincristine upregulated the expression of Bax, Bak, PUMA, Noxa, p53 and p21 proteins, and downregulated and/or phosphorylated the Bcl-2 protein. Inhibitors of the Jun N-terminal kinase (JNK), but not p38 mitogen-activated protein kinase, significantly inhibited vincristine-induced apoptosis in both IgR3 and Mel-RM cells. In addition, vincristine induced phosphorylation and reduction in Bcl-2 was prevented by an inhibitor of JNK. Downregulation of mRNA for p53, PUMA or Bim by RNA interference had little or no influence on vincristine-induced apoptosis in IgR3 cells. In addition, silencing Bim mRNA did not affect vincristine-induced apoptosis in Mel-RM cells. These results suggest that vincristine-induced apoptosis of at least some melanoma cell lines is dependent on the activation of JNK. The results are consistent with the phosphorylation of Bcl-2 protein, resulting in the activation of Bax/Bak, release of cytochrome c from the mitochondria and the resulting activation of caspases. Topics: Antineoplastic Agents, Phytogenic; Apoptosis; Apoptosis Regulatory Proteins; Bcl-2-Like Protein 11; Benzimidazoles; Blotting, Western; Carbocyanines; Caspases; Cell Line, Tumor; Dose-Response Relationship, Drug; Enzyme Activation; Flow Cytometry; Humans; JNK Mitogen-Activated Protein Kinases; Melanoma; Membrane Potential, Mitochondrial; Membrane Proteins; Mitochondrial Membrane Transport Proteins; Phosphorylation; Proto-Oncogene Proteins; Proto-Oncogene Proteins c-bcl-2; RNA, Messenger; Signal Transduction; Tubulin Modulators; Tumor Suppressor Protein p53; Vincristine	2008

Article

Year

Activation of Jun N-terminal kinase is a mediator of vincristine-induced apoptosis of melanoma cells.

Anti-cancer drugs, 2008, Volume: 19, Issue:2

The molecular changes involved in the induction of apoptosis by vincristine in melanoma have not yet been well defined. Two human melanoma cell lines showing moderate (Mel-RM) and high (IgR3) sensitivity to vincristine were selected from a panel of eight melanoma lines for analysis. Induction of apoptosis was caspase dependent, and was associated with increases in mitochondrial membrane permeability. Vincristine upregulated the expression of Bax, Bak, PUMA, Noxa, p53 and p21 proteins, and downregulated and/or phosphorylated the Bcl-2 protein. Inhibitors of the Jun N-terminal kinase (JNK), but not p38 mitogen-activated protein kinase, significantly inhibited vincristine-induced apoptosis in both IgR3 and Mel-RM cells. In addition, vincristine induced phosphorylation and reduction in Bcl-2 was prevented by an inhibitor of JNK. Downregulation of mRNA for p53, PUMA or Bim by RNA interference had little or no influence on vincristine-induced apoptosis in IgR3 cells. In addition, silencing Bim mRNA did not affect vincristine-induced apoptosis in Mel-RM cells. These results suggest that vincristine-induced apoptosis of at least some melanoma cell lines is dependent on the activation of JNK. The results are consistent with the phosphorylation of Bcl-2 protein, resulting in the activation of Bax/Bak, release of cytochrome c from the mitochondria and the resulting activation of caspases.

Topics: Antineoplastic Agents, Phytogenic; Apoptosis; Apoptosis Regulatory Proteins; Bcl-2-Like Protein 11; Benzimidazoles; Blotting, Western; Carbocyanines; Caspases; Cell Line, Tumor; Dose-Response Relationship, Drug; Enzyme Activation; Flow Cytometry; Humans; JNK Mitogen-Activated Protein Kinases; Melanoma; Membrane Potential, Mitochondrial; Membrane Proteins; Mitochondrial Membrane Transport Proteins; Phosphorylation; Proto-Oncogene Proteins; Proto-Oncogene Proteins c-bcl-2; RNA, Messenger; Signal Transduction; Tubulin Modulators; Tumor Suppressor Protein p53; Vincristine

2008