Melatonin has no effect on the growth, morphology or cell cycle of human breast cancer (MCF-7), cervical cancer (HeLa), osteosarcoma (MG-63) or lymphoblastoid (TK6) cells

Melatonin was previously shown to inhibit proliferation of MCF-7 human breast cancer cells. In this study the effect of melatonin on MCF-7 cells was further examined, while human cervical carcinoma (HeLa), osteosarcoma (MG-63) and lymphoblastoid (TK6) cells were tested for the first time. Haemocytom...

Full description

Saved in:
Bibliographic Details
Published in:Cancer letters 1998-01, Vol.122 (1), p.17-23
Main Authors: Panzer, Annie, Lottering, Mona-Lisa, Bianchi, Pepita, Glencross, Deborah K, Stark, Jenny H, Seegers, Johanna C
Format: Article
Language:English
Subjects:
Antineoplastic Agents - pharmacology
Biological and medical sciences
Breast Neoplasms - pathology
Cancer
Cell culture
Cell Cycle - drug effects
Cell Division - drug effects
DNA, Neoplasm - analysis
Dose-Response Relationship, Drug
Female
Flow Cytometry
General aspects (metabolism, cell proliferation, established cell line...)
HeLa Cells
Humans
Medical sciences
Melatonin
Melatonin - pharmacology
Osteosarcoma - pathology
Tumor cell
Tumor Cells, Cultured
Tumors
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Melatonin was previously shown to inhibit proliferation of MCF-7 human breast cancer cells. In this study the effect of melatonin on MCF-7 cells was further examined, while human cervical carcinoma (HeLa), osteosarcoma (MG-63) and lymphoblastoid (TK6) cells were tested for the first time. Haemocytometer counts, DNA content, flow cytometry and indirect immunofluorescence for nucleolar proteins, actin and β-tubulin showed no differences in the growth, cell cycle or morphology between melatonin-exposed and control cells. The direct antiproliferative effect of melatonin thus seems to be confined to a melatonin-responsive subclone of MCF-7 cells and not applicable to the majority of cancer cells.
ISSN:0304-3835
1872-7980
DOI:10.1016/S0304-3835(97)00360-1