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Antitumor effect of piericidin B1 N-oxide.

Abstract
Piericidin B1 N-oxide was isolated from a culture broth of Streptomyces sp. as a novel inhibitor of phosphatidylinositol (PI) turnover. Piericidin B1 N-oxide specifically inhibited orthophosphate labeling of PI induced by epidermal growth factor (EGF) without affecting the formation of phosphatidic acid (PA). Like piericidins A1 and B1, piericidin B1 N-oxide inhibited ATP synthesis in A431 cells; however, the effect of piericidin B1 N-oxide on PI synthesis was stronger than that of piericidins A1 and B1. At the concentration inhibiting PI synthesis, piericidin B1 N-oxide showed no inhibitory effect on DNA, RNA, or protein synthesis. We also demonstrated that piericidin B1 N-oxide reversibly inhibited the growth of A431 cells in situ and suppressed the growth of Ehrlich carcinoma in vivo when administered to mice by intraperitoneal (ip) injection.
AuthorsH Nishioka, M Imoto, T Imaoka, T Sawa, T Takeuchi, K Umezawa
JournalThe Journal of antibiotics (J Antibiot (Tokyo)) Vol. 47 Issue 4 Pg. 447-52 (Apr 1994) ISSN: 0021-8820 [Print] England
PMID8195045 (Publication Type: Journal Article)
Chemical References
  • Antibiotics, Antineoplastic
  • Cyclic N-Oxides
  • DNA, Neoplasm
  • Neoplasm Proteins
  • Phosphatidic Acids
  • Phosphatidylinositols
  • Pyridines
  • RNA, Neoplasm
  • piericidin B1 N-oxide
  • Epidermal Growth Factor
  • Adenosine Triphosphate
Topics
  • Adenosine Triphosphate (biosynthesis)
  • Animals
  • Antibiotics, Antineoplastic (pharmacology, toxicity)
  • Carcinoma, Ehrlich Tumor (drug therapy, pathology)
  • Cell Division (drug effects)
  • Cyclic N-Oxides (pharmacology, toxicity)
  • DNA, Neoplasm (biosynthesis)
  • Epidermal Growth Factor (pharmacology)
  • Humans
  • Mice
  • Neoplasm Proteins (biosynthesis)
  • Phosphatidic Acids (metabolism)
  • Phosphatidylinositols (biosynthesis)
  • Pyridines (pharmacology, toxicity)
  • RNA, Neoplasm (biosynthesis)
  • Streptomyces (metabolism)
  • Tumor Cells, Cultured

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