Abstract | BACKGROUND: MATERIALS AND METHODS: RESULTS:
DHEA dose-dependently inhibited the growth of melanoma cells and enhanced melanin production, which indicated the induction of differentiation. There was a [3H] DHEA specific binding protein in the melanoma cell cytosol. Although DHEA did not promote the translocation of PKC from the cytosolic to the membrane fraction, the total PKC activity was upregulated by treatment with DHEA. CONCLUSIONS:
DHEA inhibited the growth of B16 mouse melanoma cells by the induction of differentiation, possibly related to PKC upregulation mediated by DHEA receptor.
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Authors | S Kawai, N Yahata, S Nishida, K Nagai, Y Mizushima |
Journal | Anticancer research
(Anticancer Res)
1995 Mar-Apr
Vol. 15
Issue 2
Pg. 427-31
ISSN: 0250-7005 [Print] Greece |
PMID | 7763017
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Anticarcinogenic Agents
- Antineoplastic Agents
- Melanins
- Membrane Proteins
- Neoplasm Proteins
- Dehydroepiandrosterone
- Dexamethasone
- Protein Kinase C
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Topics |
- Animals
- Anticarcinogenic Agents
(pharmacology)
- Antineoplastic Agents
(pharmacology)
- Cell Differentiation
(drug effects)
- Cell Division
(drug effects)
- Cell Membrane
(enzymology)
- Cytosol
(enzymology)
- Dehydroepiandrosterone
(pharmacology)
- Dexamethasone
(pharmacology)
- Enzyme Induction
(drug effects)
- Melanins
(biosynthesis)
- Melanoma, Experimental
(drug therapy, pathology)
- Membrane Proteins
(metabolism)
- Mice
- Mice, Inbred C57BL
- Neoplasm Proteins
(metabolism)
- Protein Kinase C
(metabolism)
- Signal Transduction
(drug effects)
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