HER2+ breast cancer cells undergo apoptosis upon exposure to tannic acid released from remodeled cross‐linked collagen type I

Tannic acid (TA) is a naturally occurring polyphenol that cross‐links collagen type I and possesses anticancer potential. In previous studies, we demonstrated the increased sensitivity of estrogen receptor‐positive (ER+) breast cancer cells to TA as opposed to triple negative breast cancer cells and normal human breast epithelial cells. In the current study, human pre‐adipocytes and HER2+ breast cancer cells were grown on TA cross‐linked collagen type I beads. Cell attachment, growth, and proliferation of the cells result in remodeling of the collagen matrix and release of the cross‐linking TA. TA concentrations in the conditioned media were determined. Induced apoptosis of cells grown on the TA cross‐linked collagen type I beads was imaged and quantified. Viability of HER2+ breast cancer cells and normal breast epithelial cells after exposure TA released from bead remodeling was quantified. Caspase gene expression and protein expression were evaluated. HER2+ breast cancer cells underwent caspase‐mediated apoptosis in response to TA exposure. TA‐induced apoptosis in a concentration‐ and time‐dependent manner, with HER2+ breast cancer cells demonstrating an increased sensitivity to the TA effects.