期刊
FOOD & FUNCTION
卷 13, 期 8, 页码 4421-4431出版社
ROYAL SOC CHEMISTRY
DOI: 10.1039/d1fo04198c
关键词
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资金
- National Natural Science Foundation of China [81803236, 31800295]
- Natural Science Foundation of Guangdong Province [2020A1515011266, 2021A1515010958]
- 14th Five-Year Plan team-building projects of Guangdong Academy of Agricultural Sciences [202126TD]
- Guangzhou Science and Technology Plan Projects [202002030202]
- Key-Area Research and Development Program of Guangdong Province [2020B0202080003]
- Guangdong Science and Technology program [2018KJYZ002]
- Innovation Fund projects of Guangdong Key Laboratory of Tea Plant Resources Innovation and Utilization [2021CX02]
This study found that Theaflavin-3,3'-digallate (TF-3) inhibits prostate cancer cell proliferation by regulating the PKC delta/aSMase signaling pathway. The anti-prostate cancer effect of TF-3 is attributed to the expression of the 67 kDa laminin receptor (67LR).
Prostate cancer is a major cause of morbidity and mortality in men. Theaflavin-3,3 '-digallate (TF-3) is an important functional ingredient of black tea. We aimed to evaluate the cytotoxic effects of TF-3 on prostate cancer and to identify the underlying molecular mechanism. In this study, we explored the effects of TF-3 on prostate cancer in PC-3 cells and in NOD/SCID mice with prostate cancer. The results demonstrated that TF-3 inhibited prostate cancer cell proliferation by regulating the PKC delta/aSMase signaling pathway. The anti-prostate cancer effect of TF-3 was attributed to the expression of the 67 kDa laminin receptor (67LR), which is overexpressed in various cancers, playing a vital role in the growth and metastasis of tumor cells. Stable knockdown of 67LR could efficiently inhibit TF-3 induced apoptosis and cell cycle arrest in PC-3 cells, through interacting with the PKC delta/aSMase signaling pathway. In vivo studies also confirmed the above findings that TF-3 effectively inhibited tumor growth in terms of tumor volume. TF-3 treatment can significantly inhibit tumor growth and up-regulate the phosphorylation of PKC delta and the expression of aSMase in tumor xenografts developed by subcutaneously implanting PC-3 cells and 67LR-overexpressing PC-3 cells in mice. However, in tumor xenografts formed by subcutaneously implanting 67LR-knockdown PC-3 cells, TF-3 has no significant effect on PKC delta/aSMase pathway regulation and tumor growth inhibition.
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