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Published on: April 30, 2019
Selenium Induces Pancreatic Cancer Cell Death Alone and in Combination with Gemcitabine
David J Wooten1, Indu Sinha2, Raghu Sinha2
1Department of Physics, Penn State University, University Park, PA 16802, USA.
Abstract:
Survival rate for pancreatic cancer remains poor and newer treatments are urgently required. Selenium, an essential trace element, offers protection against several cancer types and has not been explored much against pancreatic cancer specifically in combination with known chemotherapeutic agents. The present study was designed to investigate selenium and Gemcitabine at varying doses alone and in combination in established pancreatic cancer cell lines growing in 2D as well as 3D platforms. Comparison of multi-dimensional synergy of combinations' (MuSyc) model and highest single agent (HSA) model provided quantitative insights into how much better the combination performed than either compound tested alone in a 2D versus 3D growth of pancreatic cancer cell lines. The outcomes of the study further showed promise in combining selenium and Gemcitabine when evaluated for apoptosis, proliferation, and ENT1 protein expression, specifically in BxPC-3 pancreatic cancer cells in vitro.
Insights
This study explores selenium and Gemcitabine for pancreatic cancer treatment. Combining these agents shows promise in reducing cancer cell growth and increasing apoptosis in vitro.
Area of Science:
- Oncology
- Trace Element Research
- Cancer Cell Biology
Background:
- Pancreatic cancer survival rates are poor, necessitating novel therapeutic strategies.
- Selenium's potential anticancer properties are recognized, but its efficacy in combination therapy for pancreatic cancer is underexplored.
- Gemcitabine is a standard chemotherapeutic agent for pancreatic cancer.
Purpose of the Study:
- To investigate the efficacy of selenium and Gemcitabine, alone and in combination, against pancreatic cancer cell lines.
- To evaluate the synergistic effects of selenium and Gemcitabine using multi-dimensional synergy (MuSyc) and highest single agent (HSA) models.
- To assess the impact of this combination on apoptosis, proliferation, and ENT1 protein expression in pancreatic cancer cells.
Main Methods:
- Culturing pancreatic cancer cell lines in 2D and 3D growth platforms.
- Administering varying doses of selenium and Gemcitabine individually and in combination.
- Utilizing MuSyc and HSA models to quantify combination synergy.
- Measuring apoptosis, proliferation, and ENT1 protein expression.
Main Results:
- The combination of selenium and Gemcitabine demonstrated synergistic effects in pancreatic cancer cell lines.
- Quantitative analysis using MuSyc and HSA models revealed improved efficacy of the combination compared to single agents.
- The combination significantly impacted apoptosis and proliferation and altered ENT1 protein expression in BxPC-3 cells.
- Observed differences in synergy between 2D and 3D cell culture models.
Conclusions:
- Selenium and Gemcitabine combination therapy holds significant promise for pancreatic cancer treatment.
- The synergistic effects observed in vitro warrant further investigation in preclinical and clinical settings.
- Understanding the impact on apoptosis, proliferation, and ENT1 expression provides mechanistic insights for this combination therapy.

