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Published on: May 3, 2021
N6-(2-hydroxyethyl)-adenosine (HEA) exhibits antitumor activity for osteosarcoma progression by regulating IGF1
Yu Dai1, Guan Huang2, Xiao Zhong3
1Department of Orthopedics, Longgang District Central Hospital of Shenzhen, Shenzhen, China.
Background:
Osteosarcoma is a highly malignant bone tumor with poor prognosis and limited treatment options due to resistance and side effects.
Objectives:
This study investigates the effects of N6-(2-hydroxyethyl)-adenosine (HEA) on osteosarcoma cells and its impact on the IGF1 signaling pathway.
Methods:
Saos2 and MG63 cell lines were treated with HEA. Cell viability, apoptosis, migration, invasion, and EMT markers were assessed. IGF1 expression was analyzed using Western blot, qPCR, and ELISA. IGF1 silencing and recombinant IGF1 treatments were used to explore HEA's mechanisms.
Results:
HEA significantly decreased osteosarcoma cell viability and induced apoptosis in a dose- and time-dependent manner. It also inhibited cell migration and invasion, and modulated EMT markers by upregulating E-cadherin and downregulating N-cadherin and vimentin. HEA downregulated IGF1 at both the mRNA and protein levels, and reduced IGF1 secretion. Furthermore, HEA inhibited the PI3K-AKT signaling pathway, which is activated by IGF1. IGF1 silencing mimicked HEA's effects, whereas recombinant IGF1 pre-treatment partially reversed HEA's effects on cell viability, apoptosis, and EMT markers.
Conclusions:
HEA exerts potent anti-cancer effects on osteosarcoma cells both in vitro and in vivo by targeting the IGF1 pathway and inhibiting downstream PI3K-AKT signaling. These results suggest that HEA holds promise as a novel therapeutic agent for osteosarcoma.
Insights
N6-(2-hydroxyethyl)-adenosine (HEA) shows significant anti-cancer effects against osteosarcoma by inhibiting the IGF1 pathway. This compound reduces tumor cell viability and metastasis, offering a promising new therapeutic avenue.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Osteosarcoma is a malignant bone tumor with limited therapeutic options.
- Drug resistance and side effects necessitate novel treatment strategies.
Purpose of the Study:
- To investigate the anti-cancer effects of N6-(2-hydroxyethyl)-adenosine (HEA) on osteosarcoma cells.
- To elucidate the role of the Insulin-like Growth Factor 1 (IGF1) signaling pathway in HEA's mechanism of action.
Main Methods:
- Osteosarcoma cell lines (Saos2, MG63) were treated with HEA.
- Assessed cell viability, apoptosis, migration, invasion, and epithelial-mesenchymal transition (EMT) markers.
- Analyzed IGF1 expression and signaling pathway (PI3K-AKT) modulation via molecular techniques.
Main Results:
- HEA significantly reduced osteosarcoma cell viability and induced apoptosis.
- HEA inhibited cell migration and invasion, modulating EMT markers (upregulating E-cadherin, downregulating N-cadherin/vimentin).
- HEA downregulated IGF1 expression and secretion, inhibiting the downstream PI3K-AKT pathway.
Conclusions:
- N6-(2-hydroxyethyl)-adenosine (HEA) demonstrates potent in vitro and in vivo anti-cancer activity against osteosarcoma.
- HEA targets the IGF1/PI3K-AKT signaling pathway, suggesting its potential as a novel therapeutic agent for osteosarcoma.
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