IGFBP-2 expression in MCF-7 cells is regulated by the PI3K/AKT/mTOR pathway through Sp1-induced increase in transcription
Abstract
Insulin-like growth factor binding protein 2 (IGFBP-2) has been implicated in the pathophysiology of neoplasia. The PI3K/AKT/mTOR pathway has recently been shown to be a predominant regulator of IGFBP-2 at the protein level in MCF-7 breast cancer cells. However, there are gaps in knowledge with respect to the molecular mechanisms that underlie this regulation. Here, we show that the PI3K/AKT/mTOR pathway regulates IGFBP-2 protein levels by modulating IGFBP-2 mRNA abundance in MCF-7 cells. This change is achieved by regulating transcription through a critical region present in the first 200 bp upstream of the transcription initiation site where Sp1 transcription factor binds and drives transcription. IGF-1 treatment leads to increased nuclear abundance of Sp1 and increased IGFBP-2 mRNA and protein levels. Rapamycin and LY294002 induce a decline in Sp1 nuclear abundance and IGFBP-2 mRNA and protein levels. This work provides a mechanistic explanation for the observed effects of the PI3K/AKT/mTOR pathway on IGFBP-2 levels in MCF-7 cells.
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TSC2−/− organoids release higher levels of IGFBP2.
“TSC2−/− organoids also released higher levels of insulin-like growth factor-binding protein 2 (IGFBP2), which is known to be regulated by mTOR in cancer cells44.”
From mTORC1 drives cell-autonomous astrocyte reactivity in tuberous sclerosis (2026) · cites this paper as [44]
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Zheng, Y., Xu, X., Lu, Z., Li, W., Wang, L., Luo, R., Xu, K., & Wang, F. (2026) · Tissue and Cell · doi:10.1016/j.tice.2026.103612
- Authors
- Mireuta, M., Darnel, A., & Pollak, M.
- Affiliations
- Jewish General Hospital (CA)
- Venue
- Growth Factors
- Publisher
- Informa UK Limited
- Published
- 2010-04-07
- Volume
- 28
- Issue
- 4
- Pages
- 243-255
- ISSN
- 0897-7194 (ISSN-L)
- 1029-2292
- OpenAlex
- W2001295103
- Cited by
- 55
- References
- 46
- Citations by year
- 2026: 3 · 2025: 2 · 2024: 2 · 2023: 2 · 2022: 4 · 2021: 4 · 2020: 1 · 2019: 4 · 2018: 4 · 2017: 2 · 2016: 2 · 2015: 7 · 2014: 4 · 2013: 5 · 2012: 6
- FWCI
- 1.82
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Growth Factors (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Growth Hormone and Insulin-like Growth Factors
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Keywords
- IGFBP-2, PI3K/AKT/mTOR pathway, Sp1, transcriptional regulation, MCF-7 cells, insulin-like growth factor I, mRNA expression, rapamycin, LY294002, promoter
- MeSH terms
- Chromones, Electrophoresis, Polyacrylamide Gel, Enzyme-Linked Immunosorbent Assay, Fluorescent Antibody Technique, Gene Expression Regulation, Humans, Morpholines, Neoplasms, Promoter Regions, Genetic, Protein Kinases, RNA, Messenger, Somatomedins, Transcription, Genetic, Blotting, Western, Signal Transduction, Gene Expression, Polymerase Chain Reaction, Sp1 Transcription Factor, Protein Serine-Threonine Kinases, Insulin-Like Growth Factor Binding Protein 2, Phosphatidylinositol 3-Kinases, Sirolimus, Cell Line, Tumor, Intracellular Signaling Peptides and Proteins, Proto-Oncogene Proteins c-akt, TOR Serine-Threonine Kinases
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