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Induction of IGF-1R expression by EGR-1 facilitates the growth of prostate cancer cells
- Source :
- Cancer letters. 317(2)
- Publication Year :
- 2011
-
Abstract
- The transcription factor Early Growth Response-1 (EGR-1) is overexpressed in human prostate tumors and contributes to prostate cancer progression through an unknown mechanism. Here we report that EGR-1 transcriptionally regulates the expression of insulin-like growth factor-1 receptor (IGF-1R), which is highly expressed in primary prostate cancer. We find that ectopic expression of EGR-1 causes increase in IGF-1R expression, while knockdown of EGR-1 leads to dramatically decrease in IGF-1R expression. Results from chromatin immunoprecipitation (ChIP) and reporter assay show that the EGR-1 directly binds to the human IGF-1R gene and triggers the target gene expression. EGR-1 activates Erk and Akt pathway through regulation of IGF-1R, and thus promote prostate cancer cell growth. Taken together, these results suggest that EGR-1 may stimulate prostate cancer cell growth through up-regulation of IGF-1R and indicate that down-regulation of EGR-1 could be an effective therapeutic approach against prostate cancer.
- Subjects :
- Male
Cancer Research
medicine.medical_specialty
Chromatin Immunoprecipitation
Blotting, Western
Biology
Receptor, IGF Type 1
Prostate cancer
Internal medicine
Cell Line, Tumor
medicine
Humans
Extracellular Signal-Regulated MAP Kinases
Transcription factor
PI3K/AKT/mTOR pathway
Cell Proliferation
Early Growth Response Protein 1
Regulation of gene expression
Gene knockdown
Binding Sites
Cell growth
Reverse Transcriptase Polymerase Chain Reaction
Prostatic Neoplasms
medicine.disease
body regions
Gene Expression Regulation, Neoplastic
Endocrinology
HEK293 Cells
Oncology
Cancer research
Ectopic expression
RNA Interference
Signal transduction
5' Untranslated Regions
Proto-Oncogene Proteins c-akt
hormones, hormone substitutes, and hormone antagonists
Protein Binding
Signal Transduction
Subjects
Details
- ISSN :
- 18727980
- Volume :
- 317
- Issue :
- 2
- Database :
- OpenAIRE
- Journal :
- Cancer letters
- Accession number :
- edsair.doi.dedup.....2e8642aec3125dc08eaa69dbb9e19664