Rhizoma Paridis Yunnanensis/Smilax aspera, Dioscorea sp. and Paris spp., e.g. Paris polyphylla
Steroid Saponins and its Sapogenins
formosanin C/Spirost-5-en-3-yl 6-deoxyhexopyranosyl-(1->2)-[6-deoxyhexopyranosyl-(1->4)-6-deoxyhexopyranosyl-(1->4)]hexopyranoside/Polyphyllin B (ForMosanin C)/PolyphyllinB/Hexopyranoside, spirost-5-en-3-yl O--6-deoxyhexopyranosyl-(1->2)-O-[O--6-deoxyhexopyranosyl-(1->4)-6-deoxyhexopyranosyl-(1->4)]-/Parissaponin Pb/Paris II/Parrisaponin/Asperin/Paris saponin II/Polyphyllin II
Formosanin C is a diosgenin saponin isolated from Paris formosana Hayata and an immunomodulator with antitumor activity. Formosanin C induces apoptosis.
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Colorectal cancer (CRC) is one of the leading causes of cancer-related morbidity and mortality worldwide. Accumulating evidence suggests that mitochondrial dynamics are closely implicated in carcinogenesis including CRC. Paris Saponin II (PSII), a major steroidal saponin extracted from Rhizoma Paris polyphylla, has emerged as a potential anticancer agent. However, the effects of PSII on CRC and its underlying mechanisms remain unknown. In the present study, we found PSII induced apoptosis and inhibited colony formation in HT 29 and HCT 116 cells, and cell cycle arrest in G1 phase. PSII inhibited the phosphorylation of ERK1/2 and mitochondrial translocation of dynamin-related protein 1 (Drp1) by dephosphorylating Drp1 at Ser616, leading to the suppression of mitochondrial fission. PSII also suppressed NF-κB activation as a result of the inhibition of IKKβ and p65 translocation. Drp1 knockdown remarkably downregulated the nuclear expression of p65 and its target genes cyclin D1 and c-Myc in HCT 116 cell, confirming the link between mitochondrial fission and NF-κB pathway. Silencing of Drp 1 enhanced the inhibitory effects of PSII on p65 phosphorylation and the expressions of cyclin D1 and c-Myc, revealing that the inhibitory effects of PSII on cyclin D1 and c-Myc were relevant in the suppression of Drp1 and NF-κB activation. An in vivo study demonstrated PSII remarkably decreased the xenograft tumor size and suppressed the phosphorylation of ERK1/2 and Drp1 at Ser616. Taken together, our results suggested that PSII could inhibit colorectal carcinogenesis, at least in part, by regulating mitochondrial fission and NF-κB pathway.
Copyright ? 2018 Elsevier Ltd. All rights reserved.
Colorectal cancer; Drp 1; Mitochondrial fission; NF-κB; Paris Saponin II; Paris Saponin II (PubChem CID: 92131287)
Paris Saponin II inhibits colorectal carcinogenesis by regulating mitochondrial fission and NF-κB pathway.
Chen M1, Ye K1, Zhang B1, Xin Q1, Li P1, Kong AN2, Wen X3, Yang J4.
Drug combination has a promising and potential development prospect in the treatment of various cancers. The objective of this study is to investigate the synergistic mechanisms of polyphyllin VII (PVII) and formosanin C (FC) in lung cancer.
MATERIALS AND METHODS:
The combination of FC and PVII influenced on the apoptosis, autophagy, and the relative signalling pathways were analysed in lung cancer cells.
The combination of FC and PVII demonstrated a concentration- dependent growth inhibition in human lung cancer cells. The combination index (CI) obtained from four lung cancer cells was smaller than 1. This synergistic antitumour effect was based on the increase of their single proapoptotic effect but inhibiting FC-induced autophagy in NCI-H460 cells. FC and PVII activated proapoptotic elements like cleaved-caspase-3, -8, and -9 to induce Beclin1 cleaved into Beclin1-C which suppressed FC-triggered autophagy and enhanced apoptosis.
Formosanin C and PVII showed a synergistic antitumour effect on lung cancer cells. The findings would provide the foundation for the use of combination drugs in the future.
? 2018 The Authors. Cell Proliferation Published by John Wiley & Sons Ltd.
The synergistic anticancer effect of formosanin C and polyphyllin VII based on caspase-mediated cleavage of Beclin1 inhibiting autophagy and promoting apoptosis.
Cui J1, Man S1, Cui N1, Yang L1, Guo Q1, Ma L1, Gao W2.
To investigate the synergistic mechanisms of Paris Saponin II (PSII) and Curcumin (CUR) in lung cancer.
MATERIALS AND METHODS:
The combination changed the cellular uptake of CUR and PSII, apoptosis, cell cycle arrest and cytokine levels were analysed on different lung cancer cells.
The combination displayed a synergistic anti-cancer effect through promoting the cellular uptake of CUR on different lung cancer cells. Hoechst H33258 staining and FACS assay indicated that the combination of PSII and CUR induced cell cycle arrest and apoptosis. Western blot and cytokine antibody microarray suggested that the combination activated death receptors such as DR6, CD40/CD40L, FasL and TNF-α to induce cancer cells apoptosis, and up-regulated IGFBP-1 leading to inhibition of PI3K/Akt pathway and increase of p21 and p27, which therefore induced a G2 phase arrest in NCI-H446 cells. Meanwhile, the combination suppressed PCNA and NF-κB pathway in 4 kinds of lung cancer cells. They activated the phosphorylation of p38 and JNK, and inhibited PI3K in NCI-H460 and NCI-H446 cells, enhanced the phosphorylation of JNK in NCI-H1299 cells, and increased the phosphorylation of p38 and ERK, and suppressed PI3K in NCI-H520 cells.
PSII combined with CUR had a synergistic anti-cancer effect on lung cancer cells. These findings provided a rationale for using the combination of curcumin and PSII in the treatment of lung cancer in future.
? 2018 John Wiley & Sons Ltd.
Paris saponin II; absorption; apoptosis; cell cycle arrest; curcumin
Curcumin enhances the anti-cancer effects of Paris Saponin II in lung cancer cells.
Man S1, Zhang L1, Cui J1, Yang L1, Ma L1, Gao W2.