In vitro antiproliferative and antioxidant effects of urolithin A, the colonic metabolite of ellagic acid, on hepatocellular carcinomas HepG2 cells

Wang, Yun; Qiu, Zhenpeng; Zhou, Benhong; Liu, Cong; Ruan, Jinlan; Yan, Qiujin; Liao, Jianming; Zhu, Fan

doi:10.1016/j.tiv.2015.04.008

Cited by 74 publications

(72 citation statements)

References 49 publications

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“…5A) and ΔΨ m collapse (Fig. 5B) suggest that p53 may inhibit cell death in ARS-treated HepG2 cells, which fits well with the observation that p53 mediates cancer cell survival during prolonged starvation through regulating autophagy in HepG2 cells [59]. In contrast, the fact that the forced expression of wild-type p53 significantly enhanced ARS-induced cytotoxicity (Fig.…”

Section: Discussionsupporting

confidence: 85%

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Artesunate induces ROS-dependent apoptosis via a Bax-mediated intrinsic pathway in Huh-7 and Hep3B cells

Pang

Qin

et al. 2016

Experimental Cell Research

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Section: Discussionsupporting

confidence: 85%

“…It was reported that ARS up-regulated p53 expression and induced p53-mediated apoptosis in HepG2 cells [18,59]. However, the evidences that PFT, a p53 inhibitor, significantly enhances ARS-induced cytotoxicity (Fig.…”

Section: Discussionmentioning

confidence: 92%

Artesunate induces ROS-dependent apoptosis via a Bax-mediated intrinsic pathway in Huh-7 and Hep3B cells

Pang

Qin

et al. 2016

Experimental Cell Research

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“…Our recent study has shown that urolithin A, one of the intestinal metabolites of ellagic acid, exerts antiproliferative and antioxidant effects in HepG2 cells through the inhibition of canonical Wnt signaling[138]. In addition, several types of antagonisms, such as peptides, small synthetic compounds, and blocking antibodies, etc .…”

Section: Resultsmentioning

confidence: 99%

Aberrant regulation of Wnt signaling in hepatocellular carcinoma

Liu

Xie

Chen

et al. 2016

WJG

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Hepatocellular carcinoma (HCC) is one of the most lethal malignancies in the world. Several signaling pathways, including the wingless/int-1 (Wnt) signaling pathway, have been shown to be commonly activated in HCC. The Wnt signaling pathway can be triggered via both catenin β1 (CTNNB1)-dependent (also known as “canonical”) and CTNNB1-independent (often referred to as “non-canonical”) pathways. Specifically, the canonical Wnt pathway is one of those most frequently reported in HCC. Aberrant regulation from three complexes (the cell-surface receptor complex, the cytoplasmic destruction complex and the nuclear CTNNB1/T-cell-specific transcription factor/lymphoid enhancer binding factor transcriptional complex) are all involved in HCC. Although the non-canonical Wnt pathway is rarely reported, two main non-canonical pathways, Wnt/planar cell polarity pathway and Wnt/Ca2+ pathway, participate in the regulation of hepatocarcinogenesis. Interestingly, the canonical Wnt pathway is antagonized by non-canonical Wnt signaling in HCC. Moreover, other signaling cascades have also been demonstrated to regulate the Wnt pathway through crosstalk in HCC pathogenesis. This review provides a perspective on the emerging evidence that the aberrant regulation of Wnt signaling is a critical mechanism for the development of HCC. Furthermore, crosstalk between different signaling pathways might be conducive to the development of novel molecular targets of HCC.

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“…Thus, some Coriobacteriaceae are able to produce equol from daidzein. These include Adlercreutzia equolifaciens [56], E. strain Julong 732, P. hongkongensis [57], S. equolifaciens [49], and S. isoflavoniconvertens [50].…”

Section: Urolithin-producing Bacteria: An Incomplete Storymentioning

confidence: 99%

Urolithins, the rescue of “old” metabolites to understand a “new” concept: Metabotypes as a nexus among phenolic metabolism, microbiota dysbiosis, and host health status

Tomás-Barberán

González‐Sarrías

Garcı́a-Villalba

et al. 2016

Molecular Nutrition Food Res

353

384

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Urolithins are dibenzo[b,d]pyran-6-one derivatives that are produced by the human gut microbiota from ellagitannins and ellagic acid (EA). These metabolites are much better absorbed than their precursors and have been suggested to be responsible for the health effects attributed to ellagitannins and EA that occur in food products as berries and nuts. In the present review, the role and potential of urolithins in human health are critically reviewed, and a perspective of the research approach needed to demonstrate these health effects is presented, based on the existing knowledge. The analytical methods available for urolithin analysis, their occurrence in different tissues and biological fluids, and their metabolism by human gut microbiota are considered. In addition, the interindividual variability observed for the production of urolithins (metabotypes) and its relationship with health status and dysbiosis are also reviewed. The potential mechanisms of action of urolithins are also critically discussed, paying attention to the concentration and the type of metabolites used in the in vitro and in vivo assays and the physiological significance of the results obtained. The gut microbiota metabolism of EA to urolithins and that of daidzein to equol, their individual variations, and the effects on health are also compared.

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In vitro antiproliferative and antioxidant effects of urolithin A, the colonic metabolite of ellagic acid, on hepatocellular carcinomas HepG2 cells

Cited by 74 publications

References 49 publications

Artesunate induces ROS-dependent apoptosis via a Bax-mediated intrinsic pathway in Huh-7 and Hep3B cells

Artesunate induces ROS-dependent apoptosis via a Bax-mediated intrinsic pathway in Huh-7 and Hep3B cells

Aberrant regulation of Wnt signaling in hepatocellular carcinoma

Urolithins, the rescue of “old” metabolites to understand a “new” concept: Metabotypes as a nexus among phenolic metabolism, microbiota dysbiosis, and host health status

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