Published March 26, 2010 | Version v1
Journal article

Leptin upregulates telomerase activity and transcription of human telomerase reverse transcriptase in MCF-7 breast cancer cells

  • 1. Key Laboratory of Breast Cancer Prevention and Therapy, Tianjin Medical University, Ministry of Education, Tianjin Medical University Cancer Hospital, Tianjin (China)

Description

The aim was to analyze the mechanism of leptin-induced activity of telomerase in MCF-7 breast cancer cells. We found that leptin activated telomerase in a dose-dependent manner; leptin upregulated the expression of Human Telomerase Reverse Transcriptase (hTERT) at mRNA and protein levels; blockade of signal transducer and activator of transcription 3 (STAT3) phosphorylation significantly counteracted leptin-induced hTERT transcription and protein expression; chromatin immunoprecipitation analysis showed that leptin enhanced the binding of STAT3 to the hTERT promoter. This study uncovers a new mechanism of the proliferative effect of leptin on breast cancer cells and provides a new explanation of obesity-related breast cancer.

Availability note (English)

Available from http://dx.doi.org/10.1016/j.bbrc.2010.02.093

Additional details

Identifiers

DOI
10.1016/j.bbrc.2010.02.093;
PII
S0006-291X(10)00313-X;

Publishing Information

Journal Title
Biochemical and Biophysical Research Communications
Journal Volume
394
Journal Issue
1
Journal Page Range
p. 59-63
ISSN
0006-291X
CODEN
BBRCA9

INIS

Country of Publication
United States
Country of Input or Organization
International Atomic Energy Agency (IAEA)
INIS RN
45023341
Subject category
S60: APPLIED LIFE SCIENCES;
Descriptors DEI
CHROMATIN; HUMAN POPULATIONS; LEPTIN; MAMMARY GLANDS; MESSENGER-RNA; METABOLIC DISEASES; NEOPLASMS; PHOSPHORYLATION; PROMOTERS; RADIATION DOSES; TRANSCRIPTION
Descriptors DEC
BODY; CHEMICAL REACTIONS; DISEASES; DOSES; GLANDS; HORMONES; NUCLEIC ACIDS; ORGANIC COMPOUNDS; ORGANS; PEPTIDE HORMONES; PEPTIDES; POLYPEPTIDES; POPULATIONS; PROTEINS; RNA

Optional Information

Copyright
Copyright (c) 2010 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.