The anti-tumor efficacy of 20(S)-protopanaxadiol, an active metabolite of ginseng, according to fasting on hepatocellular carcinoma

Li, Wenzhen; Wang, Yifan; Zhou, Xinbo; Pan, Xiaohong; Lü, Junhong; Sun, Hongliu; Xie, Zeping; Chen, Shayan; Xue, Guanhua

doi:10.1016/j.jgr.2021.06.002

Cited by 13 publications

(5 citation statements)

References 24 publications

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“…29,85,86 Considering that AMPK serves as an energy sensor and holds a crucial role in glucose sensing and energy regulation, we first screened silibinin as an optimal AMPK activator. This function is consistently with four well-known fasting mimetics, metformin, 29,87 aspirin, 39,40,88 20(S)-protopanaxadiol, 41,42 and resveratrol. 43,44 To further demonstrate that silibinin is a fasting mimetic, we determined the intracellular ATP levels and glucose consumption.…”

Section: Discussionsupporting

confidence: 63%

“…37,38 Aspirin, the inhibitor of enzyme cyclooxygenase and defined as another caloric-restriction mimetic, could inhibit non-small cell lung cancer cells and liver cancer cells growth by activating AMPK pathway. 15,39,40 Meanwhile, traditional Chinese medicine extracted compounds (such as: 20(S)-protopanaxadiol 41,42 and resveratrol 43,44 ) are detected as fasting mimetics to activate AMPK pathway. 45 Given AMPK's involvement in modulating metabolic dysregulation, mitochondrial dynamics and functions-hallmarks of cancer, AMPK presents as a promising target for cancer therapies.…”

Section: Introductionmentioning

confidence: 99%

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Silibinin, a potential fasting mimetic, inhibits hepatocellular carcinoma by triggering extrinsic apoptosis

Xiao,

Jiang,

Yuan

et al. 2024

MedComm

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Fasting, without inducing malnutrition, has been shown to have various beneficial effects, including the inhibition of tumor initiation and progression. However, prolonged fasting poses challenges for many cancer patients, particularly those in intermediate and terminal stages. Thus, there is an urgent need for the development of fasting mimetics which harness the protective effects of fasting but more suitable for patients. In this study, we first highlighted the pivotal role of silibinin in AMP‐activated protein kinase (AMPK) pathway and may serve, as a potential fasting mimetic via screening hepatoprotective drugs. Further metabolic analysis showed that silibinin inhibited the adenosine triphosphate (ATP) levels, glucose uptake and diminished glycolysis process, which further confirmed that silibinin served as a fasting mimetic. In addition, fasting synergized with silibinin, or used independently, to suppress the growth of hepatocellular carcinoma (HCC) in vivo. Mechanistically, silibinin upregulated death receptor 5 (DR5) through AMPK activation, and thus promoting extrinsic apoptosis and inhibiting HCC growth both in vitro and in vivo. Inhibition of AMPK using small interfering RNA (siRNA) or compound C, an AMPK inhibitor, significantly attenuated the upregulation of DR5 and the apoptotic response induced by silibinin. These findings suggest that silibinin holds promise as a fasting mimetic and may serve as an adjuvant drug for HCC treatment.

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Section: Discussionsupporting

confidence: 63%

Section: Introductionmentioning

confidence: 99%

Silibinin, a potential fasting mimetic, inhibits hepatocellular carcinoma by triggering extrinsic apoptosis

Xiao,

Jiang,

Yuan

et al. 2024

MedComm

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“…Another earlier study also found that INT 747 abrogated the induction of IL-6-induced EMT in an intrahepatic cholangiocarcinoma in vivo model and thereby inhibit their metastasis potential (28) . Moreover, may scientific works also showed that FMD suppressed the invasion of various cancer cells including liver and breast cancer cells (38,40) . Very few studies have investigated INT 747 anti-cancer effects in cancer therapy.…”

Section: Discussionmentioning

confidence: 98%

Role of Fasting Mimicking Diet in Farnesoid x Receptor for Suppressing Epithelial-to-Mesenchymal Transition, Cell Cycle Progression, and Viability of Prostate Cancer Cells

Wrood Salim,

Sameh Arif,

Talib Al-sudani

2023

IJPS

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The systemic and resistant nature of metastatic castration-resistant prostate cancers (mCRPC) renders it largely incurable even after intensive multimodal therapy. Proliferation, survival, and epithelial-mesenchymal transition (EMT) are three fundamental events that are deeply linked to carcinogenesis. Hence, it is necessary to find a new combination of several therapies, targeting those vital mechanisms without causing side effects. Significant research works have shown differential low expression of the metabolic Farnesoid X receptor (FXR) in primary and metastatic prostate cancer suggesting their importance in prostate pathogenesis. Obticholic acid (INT 747), a potent FXR agonist is widely used in primary biliary cholangitis, and Fasting mimicking Diet (FMD) both were drastically showed effects on different cancer progression. We hypothesized that FXR and FMD may inhibit proliferation and the metastatic phenotype in PC-3 prostate cancer cells. Analyses of the cell viability, cell cycle, migration, and matrigel invasion assays were performed to elucidate how INT 747 and /or FMD functions in prostate cancer. In this study, INT 747 treatment caused apoptotic morphological changes and significantly reduced the survival of PC-3 cells incubated in normal mediums. Furthermore, we showed that the combination of the INT 747 and FMD was much more harmful to cancer cells than the treatment with INT 747 or FMD alone. Moreover, our study showed that INT 747 either alone or combined with FMD robustly induced cell cycle arrest at the S phase. Interestingly, the combination treatment on PC-3 cells not only showed several lines of evidence of apoptotic cells death but also inhibited carcinogenic potential as evaluated by impairment of spheroid formation capacity and delayed wound healing and matrigel invasion. At the cellular level, FXR activation resulted in down-regulation of procaspase -3, vimentin, and MMP9, which triggers apoptotic cell death, cell cycle arrest, and switch from mesenchymal to an epithelial phenotype. Collectively, FXR activation alone markedly decreases, and when combined with FMD abrogates the survival and carcinogenic potential of metastatic prostate cancer cells.

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“…Preclinical and clinical studies demonstrate that fasting has a great potential for cancer therapy 11 , 46 , 47 . Evidence indicates that fasting not only induces apoptosis of cancer cells but significantly sensitizes hepatocellular carcinoma (HCC) cell to antineoplastic agents 48 , 49 , 50 . YAP hyperactivation drives initiation and progression of multiple cancer types and resistance to various targeted and chemotherapies 51 .…”

Section: Discussionmentioning

confidence: 99%

YAP regulates the liver size during the fasting-refeeding transition in mice

Fan

Cai

et al. 2023

Acta Pharmaceutica Sinica B

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The anti-tumor efficacy of 20(S)-protopanaxadiol, an active metabolite of ginseng, according to fasting on hepatocellular carcinoma

Cited by 13 publications

References 24 publications

Silibinin, a potential fasting mimetic, inhibits hepatocellular carcinoma by triggering extrinsic apoptosis

Silibinin, a potential fasting mimetic, inhibits hepatocellular carcinoma by triggering extrinsic apoptosis

Role of Fasting Mimicking Diet in Farnesoid x Receptor for Suppressing Epithelial-to-Mesenchymal Transition, Cell Cycle Progression, and Viability of Prostate Cancer Cells

YAP regulates the liver size during the fasting-refeeding transition in mice

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