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Theaflavin-3,3 '-di-gallate represses prostate cancer by activating the PKC delta/aSMase signaling pathway through a 67 kDa laminin receptor

文献类型： 外文期刊

作者： Sun, Lingli 1 ; Wen, Shuai 1 ; Li, Qiuhua 1 ; Lai, Xingfei 1 ; Chen, Ruohong 1 ; Zhang, Zhenbiao 1 ; Cao, Junxi 1 ; Sun, Shili 1 ;

作者机构： 1.Guangdong Acad Agr Sci, Tea Res Inst, Guangdong Prov Key Lab Tea Plant Resources Innova, Guangzhou 510640, Peoples R China

期刊名称：FOOD & FUNCTION （ 影响因子：6.317； 五年影响因子：6.375 ）

ISSN： 2042-6496

年卷期： 2022 年 13 卷 8 期

页码：

收录情况： SCI

摘要： 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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