Conditioned Media Derived from WJ-MSCs Enhanced the Inhibition Effect of EGCG on LNCaP Cells by Targeting Androgen Receptor and Apoptosis Pathway
International Journal of Cancer Management, ISSN: 2538-497X, Vol: 18, Issue: 1
2025
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Article Description
Background: Although there are several approaches to treat prostate cancer (PCa), the cost and side effects of some treatments pose challenges for patients. Therefore, the design of new therapeutic methods could be useful in the management of this disease. Objectives: This study aimed to investigate the synergistic effect of epigallocatechin gallate (EGCG) and conditioned medium derived from Wharton's jelly mesenchymal stem cells (WJ-MSCs) on LNCaP cells. Methods: The LNCaP cells were treated with different concentrations of EGCG and conditioned medium derived from WJ-MSCs (WJCM). The viability of treated cells was determined using the MTT assay. The expression of androgen receptor (AR and PSA) and apoptotic pathway genes (BAX, CASP3, and CASP7) were evaluated in the treated cells. Results: The analysis indicated that treatment with 400 µM EGCG in combination with 50% WJCM (0% FBS) for 72 hours decreased the expression of AR and PSA genes and enhanced the expression of BAX, CASP3, and CASP7 genes in the LNCaP cells (P < 0.05). Conclusions: The results suggest that the combination therapy of EGCG and WJCM has an anticancer effect on LNCaP cells through the activation of the apoptotic pathway and suppression of the AR pathway.
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