Silibinin: a potential old drug for cancer therapy

Ding, Ya-Hui; Wu, Yi; Qian, Lin-Yan; Zou, Hai; He, Qin

doi:10.1080/17512433.2016.1208563

Cited by 48 publications

(28 citation statements)

References 62 publications

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“…It has the major bioactive component of silymarin extracted from milk thistle (Silybum marianum) that has been used globally for decades as a traditional medicine to treat liver disorders such as chronic hepatitis and cirrhosis (Singh & Agarwal, ; Wellington & Jarvis, ). Also, inhibitory effects of silibinin on lung, prostate, liver, breast, colon, and bladder cancers have been reported (Zhu et al, ). For example, silibinin suppresses progression of prostate cancer by regulating extracellular regulated protein kinase 1/2 (ERK1/2) and transforming growth factor alpha (TGF‐α) activities (Tyagi, Sharma, Agarwal, & Agarwal, ).…”

Section: Introductionmentioning

confidence: 99%

Silibinin stimluates apoptosis by inducing generation of ROS and ER stress in human choriocarcinoma cells

Ham

Lim

Bazer

et al. 2017

Journal Cellular Physiology

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Silibinin is a flavonolignan extracted from seeds of milk thistles. Traditionally, it has been used as a therapeutic agent for liver disorders, and now it is well-known for its anti-cancer effects. However, studies on anti-cancer effects of silibinin on choriocarcinoma are very limited. Therefore, we performed proliferation and apoptosis assays to determine effects of silibinin on the viability of human choriocarcinoma (JAR and JEG3) cells. Our results showed that silibinin significantly inhibited proliferation and induced apoptosis in both JAR and JEG3 cells, and significantly increased reactive oxygen species (ROS) and lipid peroxidation. Moreover, silibinin disrupted mitochondrial function by inducing permeabilization of mitochondrial membrane potential and calcium ion efflux in JAR and JEG3 cells. Furthermore, silibinin-induced apoptosis in choriocarcinoma cells via AKT, mitogen-activated protein kinases (MAPK) and unfolded protein response (UPR) signal transduction. Collectively, our results suggest that silibinin is a novel therapeutic agent or dietary supplement for management of human placental choriocarcinomas.

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Section: Introductionmentioning

confidence: 99%

Silibinin stimluates apoptosis by inducing generation of ROS and ER stress in human choriocarcinoma cells

Ham

Lim

Bazer

et al. 2017

Journal Cellular Physiology

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“…Silibinin is a natural product that forms the major constituent of milk thistle seeds extract, and is composed of a blend of two diastereomers; silybin A and silybin B, mostly in equimolar proportions [9]. Silibinin possesses promising hepatoprotective effects; owing to its anti-oxidant and anti-inflammatory properties, and hence been utilized for management of acute and chronic liver pathologies caused by toxins, drugs and hepatitis [10]. Furthermore, in vitro studies have demonstrated anti-cancer effects against several types of cancers such as breast cancer, prostate cancer and colon cancer [9].…”

Section: Introductionmentioning

confidence: 99%

Silibinin attenuates adipose tissue inflammation and reverses obesity and its complications in diet-induced obesity model in mice

Alsaggar

Bdour

Ababneh

et al. 2020

BMC Pharmacol Toxicol

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Background: Obesity is a multifactorial chronic disease that comprises several pathological events, such as adipose hypertrophy, fatty liver and insulin resistance. Inflammation is a key contributer to development of these events, and therefore, targeting inflammation is increasingly considered for management of obesity and its complications. The aim of the current study was to investigate therapeutic outcomes of anti-inflammatory activities of the natural compound Silibinin in reversing obesity and its complication in mice. Methods: C57BL/6 male mice were fed high-fat diet for 8 weeks until development of obesity, and then injected with 50 mg/kg silibinin intraperitoneally twice per week, or vehicle for 8 weeks. Throughout the experiment, mice were continuously checked for body weight and food intake, and glucose tolerance test was performed toward the end of the experiment. Animals were sacrificed and serum and tissues were collected for biochemical, histological, and gene expression analysis to assess silibinin effects on adipose inflammation, fat accumulation, liver adipogenesis and glucose homeostasis. Results: Silibinin treatment reversed adipose tissue inflammation and adipocyte hypertrophy, and blocked progression in weight gain and obesity development with no significant effects on rates of food intake. Silibinin also reversed fatty liver disease and restored glucose homeostasis in treated animals, and reversed hyperglycemia, hyperinsulinemia and hypertriglyceridemia. Conclusion: In this study, we demonstrated that silibinin as an anti-inflammatory therapy is a potential alternative to manage obesity, as well as its related complications. Moreover, silibinin-based therapies could further evolve as a novel treatment to manage various inflammation-driven disorders.

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“…The antitumor effects of silibinin have not yet been well established, but Zhu et al . (2016) demonstrated that silibinin acts by inhibiting cell growth, proliferation, and angiogenesis and by inducing apoptosis. In nontumor cells, silibinin has shown no cytotoxic activity, suggesting selectivity to tumor cells (Tyagi et al ., 2007; Zeng et al ., 2011).…”

Section: Introductionmentioning

confidence: 99%

Inhibition of urinary bladder cancer cell proliferation by silibinin

Barros

Lima

Almeida

et al. 2020

Environ and Mol Mutagen

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Silibinin, a natural compound extracted from milk thistle, has demonstrated antitumor properties in urinary bladder cancer cells; however, the role of TP53 gene in these effects is unclear. In order to better understand the molecular and antiproliferative mechanisms of this compound, urinary bladder cancer cells with different TP53 gene status, RT4 (low-grade tumor, wild TP53 gene), 5637 (high-grade tumor, Grade 2, mutated TP53 gene), and T24 (high-grade tumor, Grade 3, mutated TP53 gene) were treated with several concentrations of silibinin (1, 5, 10, 50, 100, and 150 μM). Cytotoxicity, prooxidant effect, morphological changes, cell migration, cell cycle progression, global methylation profile, and relative expression of HOXB3, c-MYC, PLK1, SMAD4, SRC, HAT, HDAC, and RASSF1A genes were evaluated. The silibinin presented cytotoxic and prooxidant effects in the three cell lines. In mutated TP53 cells, significant interference in cell migration and cell cycle arrest at the G2/M phase was observed. Additionally, silibinin induced global DNA hypomethylation in the highest grade tumor cells. For wild-type TP53 cells, a sub-G1 apoptotic population was present. Furthermore, there was modulation of gene expression responsible for cell growth (SMAD and c-MYC), migration (SRC), cell cycle kinetics (PLK1), angiogenesis (HOXB3), and of genes associated with epigenetic events such as DNA acetylation (HAT) and deacetylation (HDAC).In conclusion, the silibinin inhibited the urinary bladder tumor cell proliferation independently of TP53 status; however, cell cycle effects, gene expression changes, and alteration of cell migration are dependent on TP53 status.

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Silibinin: a potential old drug for cancer therapy

Cited by 48 publications

References 62 publications

Silibinin stimluates apoptosis by inducing generation of ROS and ER stress in human choriocarcinoma cells

Silibinin stimluates apoptosis by inducing generation of ROS and ER stress in human choriocarcinoma cells

Silibinin attenuates adipose tissue inflammation and reverses obesity and its complications in diet-induced obesity model in mice

Inhibition of urinary bladder cancer cell proliferation by silibinin

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