Background
Resveratrol (trans-Resveratrol; SRT501) is a phytoalexin. Resveratrol is a potent reducing agent, and can prevent carcinogenesis due to its anti-oxidant abilities [1]. Resveratrol has a broad range of targets, including cyclooxygenase (e.g., COX, IC50=1.1 μM), lipoxygenase (LOC, IC50=2.7 μM), STAT3 (IC50=20 μM), and other proteins [2,3].
Resveratrol treatment is found to exert its effect on renal cell carcinoma (RCC) proliferation, migration and invasion in a concentration dependent manner through inactivation of the Akt and ERK1/2 signaling pathways [4]. In CaCo-2 cells, treatment with 25 μM Resveratrol has shown 70% growth inhibition due to S/G2 phase arrest [5]. Resveratrol treatment lead to inhibited invasion and metastasis of colorectal cancer-derived cell lines LoVo and HCT116 by suppressing the Wnt/β-catenin signaling mediated target genes of c-Myc, MMP-7, and MALT-1[6].
Resveratrol is shown to be effective against breast cancer metastasis to lungs in mice by its inhibitory effect on Stat3 mediated signaling [7]. Resveratrol treatment reduced size and number of tumor spheres in renal carcinoma stem cells xenograft mice model [8]. Resveratrol treatment reduced Epithelial to mesenchymal transition (EMT) of glioblastoma U87 xenografted mice models [9].
白藜芦醇（转-白藜芦醇；SRT501）是一种植物抗菌素。它具有强大的还原剂作用，可以通过其抗氧化能力预防致癌物质的形成[1]。 白藜芦醇具有广泛的靶点，包括环氧合酶（例如COX，IC50 = 1.1μM），脂肪氧合酶（LOC，IC50 = 2.7μM），STAT3（IC50 = 20μM）和其他蛋白质[2,3]。
翻译：研究发现，白藜芦醇治疗可以通过抑制Akt和ERK1/2信号通路的活性，在浓度依赖性下对肾细胞癌（RCC）增殖、迁移和侵袭产生影响。在CaCo-2细胞中，使用25μM的白藜芦醇处理可导致70%的生长抑制，原因是S/G2期阻滞。同时，白藜芦醇治疗还能通过抑制Wnt/β-catenin信号介导的靶基因c-Myc、MMP-7和MALT-1来抑制结直肠癌衍生细胞系LoVo和HCT116的侵袭和转移。
翻译：据显示，白藜芦醇通过抑制Stat3介导的信号传递，在小鼠乳腺癌转移至肺部方面具有一定的效果。在肾癌干细胞异种移植小鼠模型中，白藜芦醇治疗减少了肿瘤球的大小和数量。在人类胶质母细胞瘤U87异种移植小鼠模型中，白藜芦醇治疗减少了上皮向间充质转化（EMT）。
参考文献:
[1]. Bhaskara V K, Mittal B, Mysorekar V V, et al. Resveratrol, cancer and cancer stem cells: A review on past to future[J]. Current Research in Food Science, 2020, 3: 284-295.
[2]. Calamini B, Ratia K, Malkowski M G, et al. Pleiotropic mechanisms facilitated by resveratrol and its metabolites[J]. Biochemical Journal, 2010, 429(2): 273-282.
[3]. Pirola L, Fr?jd? S. Resveratrol: one molecule, many targets[J]. IUBMB life, 2008, 60(5): 323-332.
[4]. Zhao Y, Tang H, Zeng X, et al. Resveratrol inhibits proliferation, migration and invasion via Akt and ERK1/2 signaling pathways in renal cell carcinoma cells[J]. Biomedicine & Pharmacotherapy, 2018, 98: 36-44.
[5]. Schneider Y, Vincent F, Duranton B, et al. Anti-proliferative effect of resveratrol, a natural component of grapes and wine, on human colonic cancer cells[J]. Cancer letters, 2000, 158(1): 85-91.
[6]. Ji Q, Liu X, Fu X, et al. Resveratrol inhibits invasion and metastasis of colorectal cancer cells via MALAT1 mediated Wnt/β-catenin signal pathway[J]. PloS one, 2013, 8(11): e78700.
[7]. Lee-Chang C, Bodogai M, Martin-Montalvo A, et al. Inhibition of breast cancer metastasis by resveratrol-mediated inactivation of tumor-evoked regulatory B cells[J]. The Journal of Immunology, 2013, 191(8): 4141-4151.
[8]. Ji Q, Liu X, Fu X, et al. Resveratrol inhibits invasion and metastasis of colorectal cancer cells via MALAT1 mediated Wnt/β-catenin signal pathway[J]. PloS one, 2013, 8(11): e78700.
[9]. Song Y, Chen Y, Li Y, et al. Resveratrol suppresses epithelial-mesenchymal transition in GBM by regulating Smad-dependent signaling[J]. BioMed Research International, 2019, 2019.
Protocol
| Cell experiment [1]: |
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Cell lines
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ALVA-41, PC-3, and BPH-1 cells
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Preparation Method
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For cell viability studies, ALVA-41, PC-3, and BPH-1 cells were treated for 24 h with 10 μmol/L and 100 μmol/L concentrations of resveratrol or EGCG.
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Reaction Conditions
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10, 100 μM for 24 hours
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Applications
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Resveratrol at low doses (10 μmol/L) induced a proliferative response in ALVA-41 and BPH-1 cells at 24 h, which was not evident in PC-3 cells. However, at a higher dose (100 μmol/L), resveratrol produced a significant toxicity in prostate cancer cells, although the effect on ALVA-41 cells was relatively greater than on PC-3 cells.
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| Animal experiment [2]: |
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Animal models
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CB17SC mice model injected with LAPC-4 cells
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Preparation Method
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In the primary LAPC-4 study, mice were fed no resveratrol (control), 50 mg/kg/day resveratrol (RV50), or 100 mg/kg/day resveratrol (RV100).
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Dosage form
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Fed in diet, 50 mg/kg/day and 100 mg/kg/day
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Applications
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In the LAPC-4 study, RV50 significantly decreased survival while RV100 did not significantly change survival.
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参考文献:
[1]: Ahmad K A, Harris N H, Johnson A D, et al. Protein kinase CK2 modulates apoptosis induced by resveratrol and epigallocatechin-3-gallate in prostate cancer cells[J]. Molecular cancer therapeutics, 2007, 6(3): 1006-1012.
[2]: Klink J C, Tewari A K, Masko E M, et al. Resveratrol worsens survival in SCID mice with prostate cancer xenografts in a cell?\line specific manner, through paradoxical effects on oncogenic pathways[J]. The Prostate, 2013, 73(7): 754-762.
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