Session: SUN 366-382-Physiological Impacts of Endocrine Disrupting Chemicals
Poster Board SUN-368
MTS assays revealed that PG significantly induced cell death in a dose-dependent manner. HT-29 cells treated with PG displayed apoptotic features, such as cell cycle arrest at the G0/G1 phase. Consistent with this, Western blotting showed that PG treatment resulted in decreased expression of Cdk4, Cdk6 and cyclinD1, and increased expression of p27.
We observed that PG-induced apoptosis leads to the formation of the death-induced signaling complex involving Fas, FADD, procaspase-8 and AIF. These responses were accompanied by a change in the mitochondrial membrane potential along with activation of the Bcl-2 family proteins.
We also analyzed the effect of PG on the insulin-like growth factor (IGF-IR) signaling pathway. PG decreased the expressions of IGF-IR and IRS-I, and reduced the activities of mitogen-activated protein kinases (MAPKs) and ERK phosphorylation. Although further studies are required to reveal the multiple mechanisms behind the activities of PG, our findings suggest that it inhibits the proliferation of HT-29 human colon cancer cells, as observed by measuring cell death via induction of apoptosis. Therefore, PG may have therapeutic potential against the pathogenesis of colon cancer in humans.
Nothing to Disclose: TJN, MHK, MKL, IHK, YHC
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