Key result
Ellagic acid induced apoptosis and cell cycle arrest in LNCaP prostate cancer cells by modulating multiple pathways including mTOR, β-catenin, and caspase-3.
Why the study?
Does ellagic acid induce apoptosis in LNCaP human prostatic cancer cells?
Does ellagic acid induce apoptosis in LNCaP human prostatic cancer cells?
Ellagic acid induces apoptosis in LNCaP prostate cancer cells by modulating multiple apoptotic pathways, including mTOR inhibition and ROS generation.
Answers are grounded in this paper and cite their sources.
Not ready for clinical use in prostate cancer; hypothesis-generating for ellagic acid's pathway effects in cell models.
Ellagic acid (EA) inhibits cell growth and induces apoptosis in cultured cells; however, the precise molecular mechanism involved in EA-induced apoptosis in prostate cancer cells is unknown. The aim of the present study was to delineate possible apoptotic pathway(s) involved in the EA-mediated chemotherapeutic effects in the LNCaP human prostatic cancer cell line. EA produced anti-proliferative effects through inhibition of rapamycin (mTOR) activation and a reduction in intracellular levels of β-catenin. Moreover, we demonstrated that EA induced apoptosis via downregulation of the anti-apoptotic proteins, silent information regulator 1 (SIRT1), human antigen R (HuR) and heme oxygenase-1 (HO-1). EA modulated the expression of apoptosis-inducing factor (AIF) resulting in a significant increase in reactive oxygen species (ROS) levels and the activation of caspase-3. Finally, we demonstrated that EA reduced both transforming growth factor-β (TGF-β) and interleukin-6 (IL-6) levels. EA treatment resulted in the increased expression of the tumor suppressor protein p21 and increased the percentage of apoptotic cells. In conclusion, the results suggest that EA treatment represents a new and highly effective strategy in reducing prostate cancer carcinogenesis.
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Vanella et al. (2013) studied Prostate cancer. Ellagic acid vs. DMSO control was evaluated on Apoptosis and cell cycle distribution (p=<0.005). Ellagic acid induced apoptosis and cell cycle arrest in LNCaP prostate cancer cells by modulating multiple pathways including mTOR, β-catenin, and caspase-3.
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