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.2010.02.093Additional 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.