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Chemical Compound Review

Inostamycin     (2S)-2-[(2R,3S,4R,5R,6S)-5- ethyl-6-[(2R,3R...

Synonyms: LS-88495, NSC 638478, AC1L3V66, 129905-10-8
 
 
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Disease relevance of AIDS016425

 

High impact information on AIDS016425

 

Biological context of AIDS016425

  • In the present study, we examined the effects of inostamycin on cell cycle progression and apoptosis in human small cell lung carcinoma Ms-1 cells [7].
  • At a concentration of 1 microgram/ml inostamycin inhibited active [3H]vinblastine efflux from KB-C4 cells, but not from KB-3-1 cells, and inhibited [3H]vinblastine binding to KB-C4 membranes with an IC50 of 0.94 microgram/ml (1.3 microM) [8].
  • Treatment of Ms-1 cells with inostamycin, an inhibitor of phoshatidylinositol (PI) synthesis, reduced the dosage of paclitaxel required to induce cell death by apoptosis [9].
  • On the other hand, higher concentrations of inostamycin induced morphological apoptosis and DNA fragmentation in Ms-1 cells without affecting the expression of p53, Bcl-2 and Bax [7].
  • Since phosphatidylinositol (PI) 4,5-biphosphate is important for signal transduction through protein kinase C and actin reorganisation, we further examined the effect of inostamycin on production of two matrix metalloproteinases (MMPs), MMP-2 and -9, and on cell motility [1].
 

Anatomical context of AIDS016425

 

Associations of AIDS016425 with other chemical compounds

 

Gene context of AIDS016425

  • These data suggest that inostamycin reduced both proliferation and migration of HUVECs by targeting ERK-cyclin D1 and p38, respectively [11].
  • However, in the inostamycin-treated cell, cyclin-dependent kinase 2 (CDK2) failed to be activated after serum stimulation [12].
  • Inostamycin partially blocked both EGF- and phorbol 12-myristate 13-acetate-stimulated pro-MMP-9 production [1].
  • By reverse transcription-polymerase chain reaction, it was found that inostamycin diminished steady state levels of MMP-2 and -9 but not membrane type 1-MMP mRNA expressions [1].
  • Furthermore, inostamycin also inhibited cyclin D1 expression induced by serum; and consequently, hyperphosphorylation of retinoblastoma protein (pRB) by RB-kinases such as CDK4 and CDK2 was abolished, which would result in elimination of functional inactivation of pRB [12].

References

  1. Inostamycin, an inhibitor of cytidine 5'-diphosphate 1,2-diacyl-sn-glycerol (CDP-DG): inositol transferase, suppresses invasion ability by reducing productions of matrix metalloproteinase-2 and -9 and cell motility in HSC-4 tongue carcinoma cell line. Baba, Y., Tsukuda, M., Mochimatsu, I., Furukawa, S., Kagata, H., Yoji, n.u.l.l., Nagashima, n.u.l.l., Sakai, N., Koshika, S., Imoto, M., Kato, Y. Clin. Exp. Metastasis (2000) [Pubmed]
  2. Cytostatic effect of inostamycin, an inhibitor of cytidine 5'-diphosphate 1,2-diacyl-sn-glycerol (CDP-DG): inositol transferase, on oral squamous cell carcinoma cell lines. Baba, Y., Tsukuda, M., Mochimatsu, I., Furukawa, S., Kagata, H., Nagashima, Y., Koshika, S., Imoto, M., Kato, Y. Cell Biol. Int. (2001) [Pubmed]
  3. Requirement of caspase-3(-like) protease-mediated hydrogen peroxide production for apoptosis induced by various anticancer drugs. Simizu, S., Takada, M., Umezawa, K., Imoto, M. J. Biol. Chem. (1998) [Pubmed]
  4. Transmembrane domain of Bcl-2 is required for inhibition of ceramide synthesis, but not cytochrome c release in the pathway of inostamycin-induced apoptosis. Kawatani, M., Uchi, M., Simizu, S., Osada, H., Imoto, M. Exp. Cell Res. (2003) [Pubmed]
  5. Involvement of protein kinase C-regulated ceramide generation in inostamycin-induced apoptosis. Kawatani, M., Simizu, S., Osada, H., Takada, M., Arber, N., Imoto, M. Exp. Cell Res. (2000) [Pubmed]
  6. Involvement of phosphatidylinositol synthesis in the regulation of S phase induction. Imoto, M., Morii, T., Deguchi, A., Umezawa, K. Exp. Cell Res. (1994) [Pubmed]
  7. Inhibition of cyclin D1 expression and induction of apoptosis by inostamycin in small cell lung carcinoma cells. Imoto, M., Tanabe, K., Simizu, S., Tashiro, E., Takada, M., Umezawa, K. Jpn. J. Cancer Res. (1998) [Pubmed]
  8. Long-lasting accumulation of vinblastine in inostamycin-treated multidrug-resistant KB cells. Kawada, M., Umezawa, K. Jpn. J. Cancer Res. (1991) [Pubmed]
  9. Potentiation of paclitaxel cytotoxicity by inostamycin in human small cell lung carcinoma, Ms-1 cells. Simizu, S., Tanabe, K., Tashiro, E., Takada, M., Umezawa, K., Imoto, M. Jpn. J. Cancer Res. (1998) [Pubmed]
  10. Inostamycin, an inhibitor of P-glycoprotein function, interacts specifically with phosphatidylethanolamine. Kawada, M., Umezawa, K. Jpn. J. Cancer Res. (1995) [Pubmed]
  11. Inostamycin suppresses vascular endothelial growth factor-stimulated growth and migration of human umbilical vein endothelial cells. Baba, Y., Kato, Y., Mochimatsu, I., Nagashima, Y., Kurihara, M., Kawano, T., Taguchi, T., Hata, R., Tsukuda, M. Clin. Exp. Metastasis (2004) [Pubmed]
  12. Inhibition of G1 cyclin expression in normal rat kidney cells by inostamycin, a phosphatidylinositol synthesis inhibitor. Deguchi, A., Imoto, M., Umezawa, K. J. Biochem. (1996) [Pubmed]
 
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