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FBP1 induced by β-elemene enhances the sensitivity of gefitinib in lung cancer
Jian Li1, Ping Dai1, Jing Sun1
1Department of Oncology, Shanghai Fourth People's Hospital, Tongji University School of Medicine, Shanghai, China.
Background:
β-elemene is known to play a critical role in tumorigenesis as well as tyrosine kinase inhibitor (TKI) resistance in lung cancer. However, the biological function and molecular mechanism remain largely unknown.
Methods:
In this study, the common genes involved in gefitinib resistance and β-elemene were identified using bioinformatic analysis. The expression of FBP1 was examined by qRT-PCR and Western blot analysis. Cell proliferation, flow cytometry, clone formation and IC50 assays were performed to assess the effects of β-elemene and FBP1. Western blot analysis was used to evaluate apoptosis-related gene expression. Finally, in vivo experiments were conducted to assess the crucial role of FBP1 in gefitinib-resistant HCC827/GR cells in nude mice.
Results:
Screening analysis demonstrated that fructose-1,6-bisphosphatase (FBP1) was induced by β-elemene and downregulated in gefitinib-resistant lung cells. Functionally, overexpression of FBP1 inhibited proliferation and gefitinib resistance and promoted apoptosis of PC9/GR and HCC827/GR cells in vitro. Mechanistically, FBP1 impeded the nuclear translocation of p-STAT3. The FBP1/STAT3 axis was required for FBP1-mediated apoptosis-related gene expression. In vivo experiments further confirmed the enhanced effects of FBP1 on lung cancer cell sensitivity to gefitinib.
Conclusion:
Our research indicated that β-elemene suppressed proliferation and enhanced sensitivity to gefitinib by inducing apoptosis through the FBP1/STAT3 axis in gefitinib-resistant lung cancer cells.
Insights
Beta-elemene suppresses lung cancer growth and overcomes gefitinib resistance by inducing apoptosis. This occurs via the FBP1/STAT3 pathway, highlighting a novel therapeutic strategy for resistant lung cancers.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Beta-elemene plays a role in lung cancer tumorigenesis and resistance to tyrosine kinase inhibitors (TKIs).
- The precise biological functions and molecular mechanisms of beta-elemene in this context are not fully understood.
Purpose of the Study:
- To identify genes common to gefitinib resistance and beta-elemene treatment in lung cancer.
- To elucidate the molecular mechanism by which beta-elemene affects gefitinib-resistant lung cancer cells.
Main Methods:
- Bioinformatic analysis to identify common genes.
- Quantitative real-time PCR (qRT-PCR) and Western blot to examine FBP1 expression.
- In vitro assays (proliferation, flow cytometry, clone formation, IC50) and in vivo experiments in nude mice.
Main Results:
- Fructose-1,6-bisphosphatase (FBP1) was identified as upregulated by beta-elemene and downregulated in gefitinib-resistant cells.
- Overexpression of FBP1 inhibited proliferation, gefitinib resistance, and promoted apoptosis in resistant lung cancer cells.
- FBP1 impeded p-STAT3 nuclear translocation, and the FBP1/STAT3 axis mediated apoptosis-related gene expression.
Conclusions:
- Beta-elemene suppresses proliferation and enhances sensitivity to gefitinib in resistant lung cancer.
- This effect is achieved by inducing apoptosis through the FBP1/STAT3 pathway.
- FBP1 is a key mediator in beta-elemene's action against gefitinib-resistant lung cancer.
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