Article Title
Effect of 2-Deoxyglucose on Colorectal Cancer Cell Lines
Faculty Mentor
Hemachand Tummala
Abstract
The third leading cause of cancer deaths in the U.S. is colon cancer. The major disadvantage of cancer chemotherapy is its non-selective toxicity to healthy cells at the therapeutic doses. A possible target selective for cancer cells is their dependence on glycolysis for cellular energy. 2-deoxyglucose (2-DG) is a glycolytic inhibitor that has been shown to be safe in both animals and humans. The molecular mechanisms for the anticancer effect of 2-DG cannot be explained solely by its glycolytic inhibition. In this manuscript we studied the effect of 2-DG on colon cancer cells and its possible molecular mechanism. Colon cancer cells are more susceptible to 2-DG treatment than other cancerous and non-cancerous cell lines tested. The colon cancer cells tested are SW620, SW480 and GC3/C1. In cell cycle analysis studied using propidium iodide staining of DNA followed by flow-cytometry, 2-DG induced cell cycle arrest at G0/G1 phase in SW 620 cells. 2-DG also modified the expression of various cell cycle proteins such as p21, p53, and cyclins as measured through Western Blotting. In addition to cell cycle arrest, 2-DG also induced apoptosis through activation of Caspase 3. Complementing 5-Fluorouracil (5- FU) treatment of colon cancer cells with 2-DG significantly enhanced the efficiency of 5- FU treatment up to 3.5 fold. This study showed a new molecular mechanisms for 2-DG that could be used to design novel combination therapies with other known chemotherapeutic agents for colon cancer. The addition of a well-tolerated molecule like 2- DG increases the efficiency of 5-FU, thus reducing the patient’s cumulative exposure to 5- FU. This may lead to fewer dose dependent side effects and better patient outcomes.
Recommended Citation
Olinger, Alex; Muley, Pratik; and Tummala, Hemachand
(2013)
"Effect of 2-Deoxyglucose on Colorectal Cancer Cell Lines,"
The Journal of Undergraduate Research: Vol. 11, Article 5.
Available at:
https://openprairie.sdstate.edu/jur/vol11/iss1/5