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Gallic acid and its antiproliferative effect on the gastric cancer cell line MKN-28 using flow cytometry and
qPCR
Michelle Gregoire1, Felicia Talone1, Melissa Ascencao1, Songhua Zang*, Steven Moss*, Heather Axen1, JD
Swanson1
1
Salve Regina University, Dept. of Biology and biomedical sciences, Newport, RI
*Brown University, Warren Alpert Medical School, Providence RI
Background and Objective
Cancer is the second leading cause of death in the United States; gastrointestinal cancers have
particularly low survival rates. Current treatments include chemotherapy and surgery, both of which are
aggressive, non-specific, and have deleterious side effects. Gallic acid, a plant phenolic in raspberries
and blackberries, halts cellular proliferation specifically in cancer cells. This study investigates gallic
acid’s effect on cell cycle arrest and expression levels of genes important in cell cycle progression (P21,
Cdk4, Cdk6, CyclinD1), tumor angiogenesis (MMP9), and apoptosis (Bax, Bcl2, RhoB) in the immortal
gastric cancer cell line MKN-28.
Methods:
MKN-28 cells were serum starved for 48 hours to sync cell cycles and subsequently exposed to
differential dosages (0 µM, 20 µM and 100 µM) and exposure durations (0, 3, 6, 12, 24, 36 and 48 hours)
of gallic acid. Cell cycle progression was examined using flow cytometry, and changes in gene expression
were determined using qPCR.
Results
We found MKN-28 exposed to gallic acid undergoes cell cycle arrest in the G1/S phase, resulting in a
longer doubling time than the untreated 36 hours. We expected gene expression levels to increase for
genes important apoptotic pathways, and tumor angiogenesis, and to decrease in those functioning in
cell cycle regulation. Expression patterns did not match those expectations.
Discussion & conclusions
These results suggest that, gallic acid, when used as a nutraceutical, can halt proliferation of cancerous
cells and potentially reduce the negative consequences of common cancer treatments promoting a
better quality of life for cancer patients.