Inhibition of Starfish Oocyte Maturation by Tumor‐Promoting Phorbol Esters: starfish oocyte maturation/tumor promoters/phorbol esters/teleocidin/retinoids

TAKEO KISHIMOTO, Michiyasu Yoshikuni, HIROYUKI IKADAI, HARUO KANATANI

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Abstract

Effect of tumor promoters including phorbol esters and teleocidin on 1‐methyladenine (1‐MeAde)‐induced oocyte maturation was studied in the starfish. When isolated immature oocytes were treated with 1‐MeAde and 12‐O‐tetradecanoylphorbol‐13‐acetate (TPA), 1‐MeAde‐induced maturation was completely inhibited at more than 2.5 μg/ml. However, if TPA was added after the hormone‐dependent period (the minimum period wherein 1‐MeAde is required), such maturation‐inhibiting effect was no longer observed. Pretreatment with TPA for 5 min showed that its inhibitory action is irreversible. However, when TPA‐injected oocytes were treated with 1‐MeAde, all oocytes underwent germinal vesicle breakdown (GVBD). GVBD was induced in TPA‐treated oocytes upon injection of the cytoplasm of maturing oocytes containing maturation‐promoting factor (MPF). These facts show that TPA acts on the oocyte surface to inhibit the production of MPF. Retinoids including retinal, retinol and retinoic acid reversed the inhibitory effect of TPA on 1‐MeAde‐induced maturation. Experiments with various phorbol esters showed a good correlation between their maturation‐inhibiting activity and their known tumor‐promoting activity. Further, telecoidin, which is structurally unrelated to phorbol esters, inhibited 1‐MeAde action. Since both tumor‐promoting phorbol esters and teleocidin are known to activate Ca2+ ‐activated, phospholipid‐dependent protein kinase (protein kinase C) and their activation effect is inhibited by retinoids, it appears that the activation of protein kinase C by tumor promoters is involved in blocking of 1‐MeAde action.

Original languageEnglish
Pages (from-to)233-242
Number of pages10
JournalDevelopment, Growth & Differentiation
Volume27
Issue number3
DOIs
Publication statusPublished - Jan 1 1985
Externally publishedYes

Fingerprint

Starfish
Retinoids
Phorbol Esters
Carcinogens
Oocytes
Protein Kinase C
Tretinoin
teleocidins
Vitamin A
Protein Kinases
Cytoplasm
Injections

All Science Journal Classification (ASJC) codes

  • Developmental Biology
  • Cell Biology

Cite this

Inhibition of Starfish Oocyte Maturation by Tumor‐Promoting Phorbol Esters : starfish oocyte maturation/tumor promoters/phorbol esters/teleocidin/retinoids. / KISHIMOTO, TAKEO; Yoshikuni, Michiyasu; IKADAI, HIROYUKI; KANATANI, HARUO.

In: Development, Growth & Differentiation, Vol. 27, No. 3, 01.01.1985, p. 233-242.

Research output: Contribution to journalArticle

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abstract = "Effect of tumor promoters including phorbol esters and teleocidin on 1‐methyladenine (1‐MeAde)‐induced oocyte maturation was studied in the starfish. When isolated immature oocytes were treated with 1‐MeAde and 12‐O‐tetradecanoylphorbol‐13‐acetate (TPA), 1‐MeAde‐induced maturation was completely inhibited at more than 2.5 μg/ml. However, if TPA was added after the hormone‐dependent period (the minimum period wherein 1‐MeAde is required), such maturation‐inhibiting effect was no longer observed. Pretreatment with TPA for 5 min showed that its inhibitory action is irreversible. However, when TPA‐injected oocytes were treated with 1‐MeAde, all oocytes underwent germinal vesicle breakdown (GVBD). GVBD was induced in TPA‐treated oocytes upon injection of the cytoplasm of maturing oocytes containing maturation‐promoting factor (MPF). These facts show that TPA acts on the oocyte surface to inhibit the production of MPF. Retinoids including retinal, retinol and retinoic acid reversed the inhibitory effect of TPA on 1‐MeAde‐induced maturation. Experiments with various phorbol esters showed a good correlation between their maturation‐inhibiting activity and their known tumor‐promoting activity. Further, telecoidin, which is structurally unrelated to phorbol esters, inhibited 1‐MeAde action. Since both tumor‐promoting phorbol esters and teleocidin are known to activate Ca2+ ‐activated, phospholipid‐dependent protein kinase (protein kinase C) and their activation effect is inhibited by retinoids, it appears that the activation of protein kinase C by tumor promoters is involved in blocking of 1‐MeAde action.",
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