Poster No. 10
Title:
Inhibitory Effects of Rhodiola Crenulata on an Invasive Immortal Human Cell Line
Authors:
Adaris Rodríguez-Cortés, Kelly Gauger, Sallie Smith Schneider
Presented by:
Adaris Rodríguez-Cortés
Department:
Pioneer Valley Life Sciences Institute, Baystate Medical Center
Abstract:
The root of the Tibetan plant Rhodiola crenulata is part of eastern traditional medicine. Studies have suggested
that members of the Rhodiola genus display anticancer properties. In this study we examine the effect of
R. crenulata in a cellular model of invasive breast cancer, this disease being the second cause of cancer death
among women in the United States.
Deregulation of the Wnt/β-catenin pathway has been frequently observed in breast cancers and appears to have a
key role in the transformation of benign cells to a malignant form. Although mutations of the Wnt growth factor
are rarely observed in cancer, the Wnt signaling pathway is often up-regulated by either mutations that result in
stabilization of β-catenin or by hypermethylation and subsequent loss of expression of Wnt signaling antagonists
like secreted Frizzled-Related Protein 1 (SFRP1). We used an engineered cell line in which SFRP1 expression
has been knocked down. These cells were derived from 76NTert cell line, an immortalized human mammary
epithelium cell line. The resulting 76NTert-siSFRP1 cells display a mesenchymal-like phenotype, invasive
behavior and are more resistant to apoptosis triggered by anchorage independent conditions, or anoikis.
Treatment of 76NTert-siSFRP1 cells with an extract of R. crenulata inhibited migration and invasion of the
76NTert-siSFRP1 cells, as compared to untreated cells. Furthermore, R. crenulata sensitizes cells to anoikis but
does not increase γ-irradiation induced cell death. We provide evidence that death induced by R. crenulata does
not occur through the inhibition of an epithelial-to-mesenchymal transition (EMT). Taken together, our initial
results suggest R. crenulata as a potential therapeutic agent for breast cancer patients with mutations in the
Wnt/β-catenin signaling pathway.
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