In Vitro Anticancer Activity of Polysaccharide and Protein Fractions from Pithecellobium jiringa
Yanti1,2, Patricia Rika Ariani1, Widya Agustinah2
1Biology Study Program, 2Food Technology Study Program, Faculty of Biotechnology, Atma Jaya Catholic University, Jalan Jenderal Sudirman 51, Jakarta 12930, Indonesia
As one of the deadliest disease in the world, cancer has been a major health concern over the past few years. Cancer growth and development have long been associated with the overexpression of matrix metalloproteinases (MMPs), mainly MMP-2 and MMP-9. Pithecellobium jiringa (P. jiringa) or jengkol is known for its healing ability but less consumed because of its pungent smell. The aim of this research was to explore the potential anticancer activities of bioprotein and biopolysaccharide fractions of P. jiringa to be applied as potential natural agents for cancer therapy. Cell viability test was performed with A549 lung and MCF7 breast cancer cells at various concentrations (10-250 µg mL-1) to determine the optimum concentrations for cell treatments. Cell media obtained from cell treatments were collected and analysed using gelatin zymography to measure the MMP-2 and MMP-9 enzymatic activities. Real Time-PCR was performed to quantify the expression of MMP-2 and MMP-9 genes. The following six fractions from jengkol parts were extracted and tested for anticancer activity including the biopolysaccharide fraction from the seed (POB), peel (POK), seed coat (POKA) and bioprotein fraction from the seed (PRB), peel (PRK), seed coat (PRKA). MTT results demonstrated that POK fraction showed the highest inhibition at 250 μg mL-1 to MCF7 cells (66.89%) and 25 μg mL-1 to A549 cells (82.64%). Morphological features of treated cells showed signs of apoptosis. RT-PCR results indicated a significant decrease in MMP-2 gene expression and an elevated MMP-9 gene expression in cancer cells treated with bioprotein and biopolysaccharide fractions of P. jiringa. In conclusion, biopolysaccharide and bioprotein fractions of P. jiringa might kill cancer cells via downregulation of MMP-2 activity at protein and gene level, but only at protein level for MMP-9.
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