Paris saponin VII inhibits growth of colorectal cancer cells through Ras signaling pathway

Li, Yuhua; Sun, Yang; Fan, Li; Zhang, Feng; Ji, Meng; Han, Jin Xiang; Guo, Xin; Zhang, Dian; Zhang, Rong; Yue, Zhenggang; Mei, Qibing

doi:10.1016/j.bcp.2014.01.018

Cited by 59 publications

(45 citation statements)

References 30 publications

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“…Previous studies show that Polyphyllin G arrested A549 and NCI-H1299 cells in the G2/M phase [28]; Li et al point that Polyphyllin G could induce cell apoptosis, together with cell cycle arrest in G1 phase, and trigger apoptosis in a caspase-3-dependent manner in human colorectal cancer cells (HT-29 and SW-620) [42]. In this study, the flow cytometric analysis of PI-labeled cells shows that treating NPC cell lines with Polyphyllin G (4 μM) induced significant accumulation of cells in the sub-G1 phase (Figure 2B).…”

Section: Discussionmentioning

confidence: 99%

“…Previous study point that Polyphyllin G induces an autophagic cell death in HepG2 cells via inhibition of PI3K/AKT/mTOR, and activation of JNK pathway, which induces phosphorylation of Bcl-2 and dissociation of Beclin-1 from Beclin-1/Bcl-2 complex, leading to induction of autophagy [26]. Polyphyllin G inhibited cell growth by down-regulating MEK1/2, ERK1/2 phosphorylation, and suppression of AKT pathway [42]. Chen et al show that Polyphyllin G was associated with apoptosis induction and proliferation inhibition through regulation of MAPK pathway and inhibition of PI3K/Akt pathway [37].…”

Section: Discussionmentioning

confidence: 99%

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Polyphyllin G induce apoptosis and autophagy in human nasopharyngeal cancer cells by modulation of AKT and mitogen-activated protein kinase pathways in vitro and in vivo

et al. 2016

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Polyphyllin G (also call polyphyllin VII), extract from rhizomes of Paris yunnanensis Franch, has been demonstrated to have strong anticancer activities in a wide variety of human cancer cell lines. Previous studies found that Polyphyllin G induced apoptotic cell death in human hepatoblastoma cancer and lung cancer cells. However, the underlying mechanisms of autophagy in human nasopharyngeal carcinoma (NPC) remain unclear. In this study, Polyphyllin G can potently induced apoptosis dependent on the activations of caspase-8, -3, and -9 and the changes of Bcl-2, Bcl-xL and Bax protein expression in different human NPC cell lines (HONE-1 and NPC-039). The amount of both LC3-II and Beclin-1 was intriguingly increased suggest that autophagy was induced in Polyphyllin G-treated NPC cells. To further clarify whether Polyphyllin G-induced apoptosis and autophagy depended on AKT/ERK/JNK/p38 MAPK signaling pathways, cells were combined treated with AKT inhibitor (LY294002), ERK1/2 inhibitor (U0126), p38 MAPK inhibitor (SB203580), or JNK inhibitor (SP600125). These results demonstrated that Polyphyllin G induced apoptosis in NPC cells through activation of ERK, while AKT, p38 MAPK and JNK were responsible for Polyphyllin G-induced autophagy. Finally, an administration of Polyphyllin G effectively suppressed the tumor growth in the NPC carcinoma xenograft model in vivo. In conclusion, our results reveal that Polyphyllin G inhibits cell viability and induces apoptosis and autophagy in NPC cancer cells, suggesting that Polyphyllin G is an attractive candidate for tumor therapies. Polyphyllin G may promise candidate for development of antitumor drugs targeting nasopharyngeal carcinoma.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Polyphyllin G induce apoptosis and autophagy in human nasopharyngeal cancer cells by modulation of AKT and mitogen-activated protein kinase pathways in vitro and in vivo

et al. 2016

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“…Hand-Mazz. Rhizoma paridis has been reported to exert numerous pharmacological effects, including anti-inflammatory, hemostatic and anti-cancer effects, and was shown to exhibit inhibitory effects on tumor growth in numerous studies using hepatic, gastric or nasopharyngeal carcinoma models (11)(12)(13)(14)(15)(16). Furthermore, Paris saponin II significantly inhibited tumor growth by 70% in the human SKOV3 ovarian cancer xenograft model (17), and Paris saponin H showed a marked cytotoxic activity on A549 cells with an IC 50 value of 1.53±0.08 µg/ml (18).…”

Section: Introductionmentioning

confidence: 99%

Paris saponin I induces apoptosis via increasing the Bax/Bcl-2 ratio and caspase-3 expression in gefitinib-resistant non-small cell lung cancer in vitro and in vivo

Jiang

Zhao

et al. 2014

Molecular Medicine Reports

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Abstract. Polyphyllins, a major component of Rhizoma paridis, have been extensively used in non-small cell lung cancer (NSCLC). The aim of the present study was to evaluate the effects of Paris saponin I (PSI) on a panel of gefitinib-resistant NSCLC cell lines and its inhibition of tumor growth in a nude mouse model. The MTT assay was used to assess growth inhibition. The cell cycle was analyzed using flow cytometry and apoptosis was assessed using Annexin V/propidium iodide staining. The morphology of the apoptotic cells was determined by transmission electron microscopy. The protein expression levels of B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax) and caspase-3 were detected using western blot analysis. In addition, the glucose metabolism in tumor-bearing mice was evaluated using 18 F-fludeoxyglucose (FDG) micro-positron emission tomography imaging. The PSI-induced growth inhibition rate was observed to significantly increase in a time-and dose-dependent manner. Furthermore, PSI induced significant G2/M-phase arrest and apoptosis. The expression levels of Bcl-2 decreased, while those of Bax and caspase-3 increased following PSI treatment.18 F-FDG-uptake in the PSI treatment groups was significantly decreased compared with that in the control group in vivo. In conclusion, PSI is a potent antitumor agent that acts by inhibiting the proliferation of gefitinib-resistant cells, and has potential as a candidate for a natural drug for gefitinib-resistant therapy. PSI-induced apoptosis, which occurred via multiple pathways, including G2/M-phase arrest and upregulation of the Bax/Bcl-2 ratio and caspase-3 expression, ultimately led to cell death and tumor inhibition.

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“…Honokiol [65], magnolol [66], podophyllotoxin, silibinin, hydnocarpin Substances other than polyphenols Alkaloids Antofine [67,68], avenanthramide, neo-clerodane diterpenoid alkaloids, taspine Terpenes Maslinic acid [69], talaporfin, novel triterpenoids, ent-clerodane diterpenoids, curcuphenol, picrotoxin, solaniol, triptolide, carnosic acid, koetjapic acid, andrographolide, plaunotol, geranylgeraniol Sapogenin Yerba mate tea and mate saponins [70], Paris saponin VII [71] Other substances Polyacetylenes and polyenes [72], chromane derivatives [73], grifolin [74], g-oryzanol [75], yuanhuacine [76], chartreusin [77], simvastatin and lovastatin [78], TPU942 and its derivatives [79], PTZ0025, phytic acid, b-sitosterol, diallyl sulfide, brefeldin A, parthenolide, norcantharidin, protopanaxadiol, melanoidin, evodiamine, 1'-acetoxychavicol acetate, panaxadiol, renieramycin, pyrazolone derivatives, b-asarone, phthalide, turmerone…”

Section: Polyphenolsmentioning

confidence: 99%

The use of natural products in colorectal cancer drug discovery

Miura

Satoh

Kinouchi

et al. 2015

Expert Opinion on Drug Discovery

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Paris saponin VII inhibits growth of colorectal cancer cells through Ras signaling pathway

Cited by 59 publications

References 30 publications

Polyphyllin G induce apoptosis and autophagy in human nasopharyngeal cancer cells by modulation of AKT and mitogen-activated protein kinase pathways in vitro and in vivo

Polyphyllin G induce apoptosis and autophagy in human nasopharyngeal cancer cells by modulation of AKT and mitogen-activated protein kinase pathways in vitro and in vivo

Paris saponin I induces apoptosis via increasing the Bax/Bcl-2 ratio and caspase-3 expression in gefitinib-resistant non-small cell lung cancer in vitro and in vivo

The use of natural products in colorectal cancer drug discovery

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