Further Elucidation of the Role of Protein Kinase-C and Rho Kinase in the Mechanism of Action of Bitter Melon Extract on Human Metastatic Breast Cancer Cells

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Bhupal P. Bhetwal Ph.D

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Medicine and Health Sciences


Introduction: It is well documented in the literature that Bitter Melon Extract (BME) inhibits the growth and proliferation of MCF-7 breast cancer cells. While the exact mechanism of this inhibition is unknown, it is possible that Protein Kinase C (PKC) and Rho Kinase (ROK) play a role in this mechanistic pathway due to their known critical roles in cell migration, division, and survival. Previous research has shown that ROK inhibition results in decreased cell viability and decreased MYPT1 (Myosin phosphatase targeting subunit-1) expression, while PKC inhibition alone does not have a significant effect. Aims: The aim of this research is to investigate the cytotoxic mechanism of action enacted by BME on MCF-7 cells and how PKC and ROK might be involved in this mechanism by building on past research to create more robust data and a better understanding of the metabolic state of MCF-7 cells under the set conditions. Methods: Glucose assays were run via a GM-100 glucometer to test for cell metabolism as a measure of cell viability on BME dose (0%, 0.5%, 1%, 2%, 5%, and 10% BME (v/v)) study samples, PKC inhibitor (GF109203x; 0.5 uM) samples, and ROK inhibitor (H-1152; 1 uM) samples. The samples used in each of the three conditions were secured from past research. Results & Discussion: BME dose-dependently increased glucose remaining in the culture media. The sample sizes for different doses of BME were as follows; at 0% (n=4), 0.5% (n=5), and 1% (n=5), while 2% (n=2), 5% (n=3), and 10% (n=3). The data suggests two possibilities; (i) with increasing BME dose, there is an increasing effect on the MCF-7 cell’s metabolism of glucose, and that this decrease in ability to metabolize glucose when in the presence of increasing [BME] could play a role in the cytotoxic mechanism of BME on MCF-7 cells. (ii) The BME kills cells and hence glucose is not used as much thus leaving plenty of glucose in the medium. Our results further showed that neither PKC inhibitor samples (n= 7) nor ROK inhibitor samples (n=11) showed significant differences in [glucose]. This suggests that the measured effect in glucose metabolism in the BME dose-dependent study samples is independent of PKC and ROK mechanistic pathways.


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