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Downregulation of basic fibroblast growth factor increases cisplatin sensitivity in A549 non-small cell lung cancer
Long He1, Yousheng Meng2, Zhihui Zhang2
1Department of Medical Oncology, Qilu Hospital of Shandong University; Department of Medical Oncology, The Third Hospital of Jinan, Jinan, Shandong, China.
Objectives:
The objective of the study is to investigate the role of basic fibroblast growth factor (bFGF) in sensitivity to cisplatin in non-small cell lung cancer (NSCLC) A549 cells and its effect on the stemness characteristics of NSCLC cells, revealing possible mechanisms of cisplatin resistance.
Materials And Methods:
After A549 cells were treated with cisplatin, bFGF protein expression was analyzed by Western blot. A549 cells were transfected with bFGF small interfering RNAs (siRNAs), and the knockdown efficiency was confirmed by quantitative reverse transcription polymerase chain reaction and Western blot. After bFGF downregulation, A549 cell proliferation was assessed by Cell Counting Kit-8 assay. The effect of bFGF siRNA on the sensitivity to cisplatin was evaluated by cell viability assays and flow cytometry for cell apoptosis. Colony formation assay was performed to explore whether bFGF affected the stemness characteristics of A549 cells, and OCT-4 protein expression was analyzed by Western blot after bFGF siRNA treatment.
Results:
Cisplatin treatment enhanced bFGF expression in A549 cells. After A549 cells were transfected with bFGF siRNAs, bFGF expression was significantly decreased compared to that in the negative control siRNA group. In addition, bFGF knockdown inhibited A549 cell proliferation. bFGF siRNA treatment enhanced the inhibitory effect of different concentrations of cisplatin on cell viability and promoted cisplatin-induced apoptosis in A549 cells. Further analyses showed that bFGF siRNA treatment not only significantly decreased colony formation in A549 cells but also downregulated OCT-4 protein expression.
Conclusion:
bFGF decreased NSCLC sensitivity to cisplatin in vitro, while it enhanced colony formation ability and increased OCT-4 expression of A549 cells, which might account for its involved mechanisms of cisplatin resistance.
Insights
Basic fibroblast growth factor (bFGF) reduces non-small cell lung cancer (NSCLC) cell sensitivity to cisplatin. Downregulating bFGF enhances cisplatin efficacy and reduces cancer stemness markers like OCT-4.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Non-small cell lung cancer (NSCLC) remains a leading cause of cancer mortality.
- Cisplatin is a cornerstone chemotherapy, but resistance limits its efficacy.
- Cancer stemness characteristics are implicated in therapeutic resistance.
Purpose of the Study:
- To investigate the role of basic fibroblast growth factor (bFGF) in cisplatin sensitivity of NSCLC A549 cells.
- To determine bFGF's effect on stemness characteristics in NSCLC.
- To elucidate potential mechanisms of cisplatin resistance mediated by bFGF.
Main Methods:
- A549 cells were treated with cisplatin, and bFGF expression was analyzed.
- bFGF was downregulated using small interfering RNAs (siRNAs).
- Cell proliferation, apoptosis, colony formation, and OCT-4 expression were assessed.
Main Results:
- Cisplatin treatment increased bFGF expression in A549 cells.
- bFGF knockdown inhibited cell proliferation and enhanced cisplatin-induced apoptosis.
- Reduced bFGF decreased colony formation and downregulated OCT-4 expression.
Conclusions:
- bFGF diminishes NSCLC sensitivity to cisplatin in vitro.
- bFGF enhances NSCLC colony formation and OCT-4 expression, contributing to cisplatin resistance.
- Targeting bFGF may represent a strategy to overcome cisplatin resistance in NSCLC.
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