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FoxM1 is a novel target of a natural agent in pancreatic cancer
Zhiwei Wang1, Aamir Ahmad, Sanjeev Banerjee
1Department of Pathology, Karmanos Cancer Institute, Wayne State University School of Medicine, 740 HWCRC, 4100 JohnR Street, Detroit, Michigan 48201, USA.
Purpose:
Pancreatic cancer remains the fourth most common cause of cancer-related death in the United States. Therefore, novel strategies for the prevention and/or treatment are urgently needed. Genistein has been found to be responsible for lowering the rate of pancreatic cancer. However, the molecular mechanisms by which genistein elicits its effects on pancreatic cancer cells has not been fully elucidated. Therefore, the purpose of the current study was to elucidate the anti-cancer mechanism(s) of genistein.
Methods:
Multiple molecular techniques, such as Real-time RT-PCR, Western blot analysis, invasion assay, immunofluorescence assay, gene transfection, MTT assay, and Histone/DNA ELISA, were used.
Results:
We found that genistein inhibited cell growth accompanied by induction of apoptosis with concomitant attenuation of FoxM1 and its downstream genes, such as survivin, cdc25a, MMP-9, and VEGF, resulting in the inhibition of pancreatic cancer cell invasion. We also found that down-regulation of FoxM1 by siRNA prior to genistein treatment resulted in enhanced cell growth inhibition and induction of apoptosis.
Conclusion:
This is the first report showing the molecular role of FoxM1 in mediating the biological effects of genistein in pancreatic cancer cells, suggesting that FoxM1 could be a novel target for the treatment of pancreatic cancer.
Insights
Genistein, a compound found in soy, inhibits pancreatic cancer growth by reducing the expression of FoxM1 (Forkhead box protein M1) and its target genes. This mechanism enhances apoptosis and reduces cancer cell invasion.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Pancreatic cancer is a leading cause of cancer death in the US.
- Novel prevention and treatment strategies are urgently needed.
- Genistein shows promise in lowering pancreatic cancer rates, but its mechanisms are unclear.
Purpose of the Study:
- To elucidate the anti-cancer molecular mechanisms of genistein in pancreatic cancer cells.
- To investigate the role of genistein in regulating key cancer-related genes.
- To identify potential therapeutic targets for pancreatic cancer treatment.
Main Methods:
- Utilized molecular techniques including Real-time RT-PCR, Western blot, invasion assays, immunofluorescence, gene transfection, MTT assay, and Histone/DNA ELISA.
- Employed siRNA to down-regulate FoxM1 expression.
- Analyzed the impact of genistein on cell growth, apoptosis, and invasion.
Main Results:
- Genistein inhibited pancreatic cancer cell growth and induced apoptosis.
- Genistein treatment led to the attenuation of FoxM1 and its downstream genes (survivin, cdc25a, MMP-9, VEGF).
- Down-regulation of FoxM1 enhanced genistein's inhibitory effects on cell growth and apoptosis.
Conclusions:
- This study identifies the molecular role of FoxM1 in mediating genistein's anti-cancer effects in pancreatic cancer.
- FoxM1 is a key mediator of genistein's ability to inhibit pancreatic cancer cell growth, apoptosis, and invasion.
- FoxM1 represents a potential novel therapeutic target for pancreatic cancer treatment.
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