In vitro and in vivo anticancer efficacy of silibinin against human pancreatic cancer BxPC-3 and PANC-1 cells

Nambiar, Dhanya K.; Prajapati, Vandana; Agarwal, Rajesh; Singh, Rana P.

doi:10.1016/j.canlet.2012.09.004

Cited by 48 publications

(39 citation statements)

References 32 publications

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“…After 6, 12 and 24 h of these treatments, total cells were collected by brief trypsinization, and washed with phosphate-buffered saline (PBS) twice. Live cell number was determined by trypan blue dye exclusion assay (Agarwal et al, 2003; Nambiar et al, 2012). Each treatment and time point had three independent plates.…”

Section: Methodsmentioning

confidence: 99%

“…The effect of NaBt treatment on cell cycle distribution was determined by flow cytometry after staining the cells with propidium iodide (PI) as described earlier (Nambiar et al, 2012; Stan et al, 2008)). Briefly, 1 × 10 5 cells were seeded, allowed to attach by overnight incubation, and exposed to desired concentrations of NaBt for specified time periods.…”

Section: Methodsmentioning

confidence: 99%

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Sodium butyrate induces DRP1-mediated mitochondrial fusion and apoptosis in human colorectal cancer cells

et al. 2014

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Sodium butyrate (NaBt) is the byproduct of anaerobic microbial fermentation inside the gastro-intestinal tract that could reach upto 20 mM, and has been shown to inhibit the growth of various cancers. Herein, we evaluated its effect on mitochondrial fusion and associated induction of apoptosis in colorectal cancer cells (CRC). NaBt treatment at physiological (1-5 mM) concentrations for 12 and 24 h decreased the cell viability and induced G2-M phase cell cycle arrest in HCT116 (12h) and SW480 human CRC cells. This cell cycle arrest was associated with mitochondria-mediated apoptosis accompanied by a decrease in survivin and Bcl-2 expression, and generation of reactive oxygen species (ROS). Furthermore, NaBt treatment resulted in a significant decrease in the mitochondrial mass which is an indicator of mitochondrial fusion. Level of dynamin-related protein 1 (DRP1), a key regulator of mitochondrial fission and fusion where its up-regulation correlates with fission, was found to be decreased in CRC cells. Further, at early treatment time, DRP1 down-regulation was noticed in mitochondria which later became drastically reduced in both mitochondria as well as cytosol. DRP1 is activated by cyclin B1-CDK1 complex by its ser616 phosphorylation in which both cyclin B1-CDK1 complex and phospho-DRP1 (ser616) were strongly reduced by NaBt treatment. DRP1 was observed to be regulated by apoptosis as pan-caspase inhibitor showing rescue from NaBt-induced apoptosis also caused the reversal of DRP1 to the normal level as in control proliferating cells. Together, these findings suggest that NaBt can modulate mitochondrial fission and fusion by regulating the level of DRP1 and induce cell cycle arrest and apoptosis in human CRC cells.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Sodium butyrate induces DRP1-mediated mitochondrial fusion and apoptosis in human colorectal cancer cells

et al. 2014

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“…In addition, silibinin is also found to display various biological activities including anti-oxidative, anti-proliferative, anti-bacterial, anti-fungal, neuro-protective, anti-leishmanial, anti-osteoclastic and anti-metastatic activities [310][311][312][313][314][315][316][317]. Previous studies have reported that silibinin exerts remarkable effects in numerous cancers such as renal, hepatocellular and pancreatic carcinoma, bladder, breast, colorectal, ovarian, lung, salivary gland, prostate and gastric cancers, through the induction of apoptosis, inhibition of tumor growth, metastasis and angiogenesis [318][319][320][321][322][323][324][325][326][327][328].…”

Section: Silibininmentioning

confidence: 99%

Naturally occurring anti-cancer compounds: shining from Chinese herbal medicine

et al. 2019

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Numerous natural products originated from Chinese herbal medicine exhibit anti-cancer activities, including antiproliferative, pro-apoptotic, anti-metastatic, anti-angiogenic effects, as well as regulate autophagy, reverse multidrug resistance, balance immunity, and enhance chemotherapy in vitro and in vivo. To provide new insights into the critical path ahead, we systemically reviewed the most recent advances (reported since 2011) on the key compounds with anti-cancer effects derived from Chinese herbal medicine (curcumin, epigallocatechin gallate, berberine, artemisinin, ginsenoside Rg3, ursolic acid, silibinin, emodin, triptolide, cucurbitacin B, tanshinone I, oridonin, shikonin, gambogic acid, artesunate, wogonin, β-elemene, and cepharanthine) in scientific databases (PubMed, Web of Science, Medline, Scopus, and Clinical Trials). With a broader perspective, we focused on their recently discovered and/or investigated pharmacological effects, novel mechanism of action, relevant clinical studies, and their innovative applications in combined therapy and immunomodulation. In addition, the present review has extended to describe other promising compounds including dihydroartemisinin, ginsenoside Rh2, compound K, cucurbitacins D, E, I, tanshinone IIA and cryptotanshinone in view of their potentials in cancer therapy. Up to now, the evidence about the immunomodulatory effects and clinical trials of natural anti-cancer compounds from Chinese herbal medicine is very limited, and further research is needed to monitor their immunoregulatory effects and explore their mechanisms of action as modulators of immune checkpoints.

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“…In addition, silibinin reduced vascular endothelial growth factor (VEGF) secretion, metalloproteinase-2 (MMP-2), and CD34 in hepatic cancer cells suggesting inhibition of angiogenesis in hepatic tumors (29,30). In pancreatic cancer cell lines, silibinin inhibited their proliferation in a dose-and time-dependent fashion which translated to a decrease in tumor marianum; Asteraceae volume in a mouse xenograft model (32). Again, this inhibition appeared to be a function of both increased apoptosis as well as cell cycle arrest by silibinin.…”

Section: Broad Spectrum Cancer Chemopreventive Efficacy Of Silibininmentioning

confidence: 99%

Molecular Mechanisms of Silibinin-Mediated Cancer Chemoprevention with Major Emphasis on Prostate Cancer

Ting

Deep

Agarwal

2013

AAPS J

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Abstract. Despite advances in early detection, prostate cancer remains the second highest cancer mortality in American men, and even successful interventions are associated with enormous health care costs as well as prolonged deleterious effects on quality of patient life. Prostate cancer chemoprevention is one potential avenue to alleviate these burdens. It is a regime whereby long-term treatments are intended to prevent or arrest cancer development, in contrast to more direct intervention upon disease diagnosis. Based on this intention, cancer chemoprevention generally focuses on the use of nontoxic chemical agents which are well-tolerated for prolonged usage that is necessary to address prostate cancer's multistage and lengthy period of progression. One such nontoxic natural agent is the flavonoid silibinin, derived from the milk thistle plant (Silybum marianum), which has ancient medicinal usage and potent antioxidant activity. Based on these properties, silibinin has been investigated in a host of cancer models where it exhibits broad-spectrum efficacy against cancer progression both in vitro and in vivo without noticeable toxicity. Specifically in prostate cancer models, silibinin has shown the ability to modulate cell signaling, proliferation, apoptosis, epithelial to mesenchymal transition, invasion, metastasis, and angiogenesis, which taken together provides strong support for silibinin as a candidate prostate cancer chemopreventive agent.

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In vitro and in vivo anticancer efficacy of silibinin against human pancreatic cancer BxPC-3 and PANC-1 cells

Cited by 48 publications

References 32 publications

Sodium butyrate induces DRP1-mediated mitochondrial fusion and apoptosis in human colorectal cancer cells

Sodium butyrate induces DRP1-mediated mitochondrial fusion and apoptosis in human colorectal cancer cells

Naturally occurring anti-cancer compounds: shining from Chinese herbal medicine

Molecular Mechanisms of Silibinin-Mediated Cancer Chemoprevention with Major Emphasis on Prostate Cancer

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