<i>In Vivo</i> and <i>In Vitro</i> Antitumor Effects of Platycodin D, a Saponin Purified from Platycodi Radix on the H520 Lung Cancer Cell

Park, Jae Chan; Lee, Young Joon; Choi, Hae Yun; Shin, Yong Kook; Kim, Jong Dae; Ku, Sae Kwang

doi:10.1155/2014/478653

Cited by 22 publications

(31 citation statements)

References 68 publications

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“…As the principal active component in Platycodonis Radix, PD has been confirmed to have potential anticancer effects by inhibiting proliferation, inducing apoptosis, inducing cell cycle arrest, and blocking metastasis [9,10,[13][14][15]37] . This study provided evidence that PD inhibits cell proliferation of human hepatocellular carcinoma However, a decrease in body weight was observed during 10 mg/kg PD treatment ( Figure 2C).…”

Section: Discussionmentioning

confidence: 99%

“…In addition, two mice died in the 10 mg/kg and 5 mg/kg PD-treated groups during the 21 d period, revealing that the intraperitoneal treatment with PD had toxic effects in BEL-7402 xenograft mice. More recently, oral administration of PD (50, 100, and 200 mg/kg) has been reported to reduce the tumor volumes in lung cancer H520 cell-bearing nude mice [37] . Thus, different administration methods of PD should be taken into consideration.…”

Section: Discussionmentioning

confidence: 99%

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Platycodin D induces apoptosis and triggers ERK- and JNK-mediated autophagy in human hepatocellular carcinoma BEL-7402 cells

Tang

et al. 2015

Acta Pharmacol Sin

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Aim: Platycodin D, the main saponin isolated from Chinese herb Platycodonis Radix, exhibits anticancer activities against various cancer cell lines. Here we evaluated its anticancer action against human hepatocellular carcinoma cells in vitro and in vivo, and elucidated the relationship between platycodin D-induced apoptosis and autophagy. Methods: The viability of human hepatocellular carcinoma BEL-7402 cells was evaluated with MTT assay, and the apoptosis was examined using Annexin V/PI and Hoechst 33342 staining assays. Monodansylcadaverine (MDC) staining was used to label autophagic vacuoles. The proteins were detected using Western blot analysis. For studying its anticancer action in vivo, platycodin D (5 and 10 mg·kg -1 ·d -1 ) was intraperitoneally injected to BEL-7402-bearing mice for 21 days.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Platycodin D induces apoptosis and triggers ERK- and JNK-mediated autophagy in human hepatocellular carcinoma BEL-7402 cells

Tang

et al. 2015

Acta Pharmacol Sin

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“…As reported by Park et al (2014) that PD in dosages of 50, 100, and 200 mg/kg exerted noticeable immunological enhancement and anti-cachexia effects on H520 tumor cell-bearing mice. In the present investigation, our results also showed that the thymus and spleen indices in all PD groups had no great significance compared to the vehicle control group.…”

Section: Discussionmentioning

confidence: 52%

Platycodin D exerts anti-tumor efficacy in H22 tumor-bearing mice via improving immune function and inducing apoptosis

Tian

Liu

et al. 2016

J. Toxicol. Sci.

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-Platycodin D (PD), a major saponin derived and isolated from the roots of Platycodon grandiflorum, exerts potent growth inhibition and strong cytotoxicity against various cancer cell lines. However, the anti-tumor efficacy of PD on H22 hepatocellular carcinoma remains unknown. In the present study, we aimed to explore the anti-hepatoma activity in vivo and the underlying mechanism of PD in H22 tumor-bearing mice. The results revealed that PD could considerably suppress tumor growth with no significant side effects on immune organs and body weight. Further investigations showed that the levels of serum cytokines, including interferon gamma (IFN-γ), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-2 (IL-2), were enhanced by PD administration. On the other hand, PD inhibited the production of vascular endothelial growth factor (VEGF) in serum of H22 tumor mice. Additionally, the observations from H&E and Hoechst 33258 staining results demonstrated that PD noticeably induced apoptosis in H22 hepatocellular carcinoma cells. Importantly, immunohistochemical analysis showed that PD treatment increased Bax expression and decreased Bcl-2 and VEGF expression of H22 tumor tissues in a dose-dependent manner. Taken together, the findings in the present investigation clearly demonstrated that the PD markedly suppressed the tumor growth of H22 transplanted tumor in vivo at least partly via improving the immune functions, inducing apoptosis, and inhibiting angiogenesis.

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“…As the most abundant triterpenoid saponin derived from the roots of Platycodin grandiflorum, Platycodin D (PD), has been reported to show a wide range of health benefits, such as anti-atherosclerotic (4), anti-inflammatory (5,6), hypocholesterolemic and anti-obesity effects (7). Previous studies have shown that PD has obvious anticancer activity against different human malignant cancer cells both in vitro (10,11,13,14,16,17) and in vivo (9,12,15).…”

Section: Discussionmentioning

confidence: 99%

“…Platycodin D (PD), a triterpenoid saponin derived from the roots of Platycodin grandiflorum, has been reported to possess a wide rangeof health benefits, such as anti-atherosclerotic (4), anti-inflammatory (5,6), hypocholesterolemic, and anti-obesity effects (7), as well as spermicidal and contraceptive activity (8). Among the various health benefits of PD, anticancer effects have been noted in several cancer cell lines, including lung cancer cells (9), hepatocellular carcinoma cells (10), gastric cancer cells (11), prostate cancer cells (12), and leukemia cells (13,14). PD has also been reported to inhibit the viability of human breast cancer cells in vitro (15)(16)(17).…”

Section: Introductionmentioning

confidence: 99%

Platycodin D, a metabolite of Platycodin grandiflorum, inhibits highly metastatic MDA-MB-231 breast cancer growth in vitro and in vivo by targeting the MDM2 oncogene

Kong

Wang

et al. 2016

Oncology Reports

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Abstract. The objective of the present study was to explore the in vitro and in vivo anticancer effects of Platycodin D (PD), derived from Platycodin grandiflorum, on highly metastatic MDA-MB-231 breast cancer cells. Using the MTT assay, we found that PD inhibited MDA-MB-231 cell growth in a concentration-dependent manner, with an IC 50 value of 7.77±1.86 µM. Further studies showed that PD had antiproliferative effects and induced cell cycle arrest in the G0/G1 phase. To explore the detailed mechanism(s) by which PD suppressed MDA-MB-231 cell growth, western blot analyses were used to detect the expression levels of proteins related to cell proliferation and survival. The data showed that PD decreased the expression of proteins related to the G0/G1 phases, downregulated the protein expression of MDM2, MDMX, and mutant p53, and increased the expression levels of p21 and p27 in vitro. We verified the effects of PD on the expression of MDM2, MDMX, mutant p53, p21 and p27 using a pcDNA3-Flag-MDM2 plasmid and MDM2 siRNA transfection, and found that PD inhibited MDA-MB-231 cell viability by targeting MDM2 and mutant p53. Compared with the corresponding parental cells, the cells with siRNA-MDM2 transfection had a greater decrease in cell viability and proliferation, while those with pcDNA3-MDM2 plasmid transfection did not show any increase in the effects of PD. We also established a MDA-MB-231 xenograft model in BALB/c nude mice, and found that PD significantly inhibited the growth of MDA-MB-231 xenograft tumors in these mice. The expression levels of various proteins in the tumor tissue exhibited changes similar to those observed in vitro. These findings indicate that PD exerted in vitro and in vivo anticancer effects against MDA-MB-231 breast cancer cells, that PD is a potential MDM2/MDMX inhibitor, and that the anticancer effects of PD were likely associated with its inhibition of these proteins. Our observations help to identify a mechanism by which PD functions as an anti-breast cancer agent. IntroductionBreast cancer is the most frequently diagnosed malignancy and the leading cause of cancer death among females worldwide, accounting for 25% of all cancer cases and 15% of the total cancer deaths in 2012 (1). According to the American Cancer Society, about 231,840 new cases of invasive breast cancer and approximately 60,290 new cases of carcinoma in situ would occur in the US in 2015 (2). To relieve the huge burden of cancer therapy and promote women's health, there is an urgent need to discover new drugs to treat breast cancer.Natural products, such as thymoquinone, wogonin, naphtho, and quercetin, have been shown to possess different anticancer functions, such as the induction of cell cycle arrest, suppression of tumor angiogenesis, and inhibition of cell migration or invasion (3). Platycodin D (PD), a triterpenoid saponin derived from the roots of Platycodin grandiflorum, has been reported to possess a wide rangeof health benefits, such as anti-atherosclerotic (4), anti-inflammatory (5,6), hypocholesterolemic, ...

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In Vivo and In Vitro Antitumor Effects of Platycodin D, a Saponin Purified from Platycodi Radix on the H520 Lung Cancer Cell

Cited by 22 publications

References 68 publications

Platycodin D induces apoptosis and triggers ERK- and JNK-mediated autophagy in human hepatocellular carcinoma BEL-7402 cells

Platycodin D induces apoptosis and triggers ERK- and JNK-mediated autophagy in human hepatocellular carcinoma BEL-7402 cells

Platycodin D exerts anti-tumor efficacy in H22 tumor-bearing mice via improving immune function and inducing apoptosis

Platycodin D, a metabolite of Platycodin grandiflorum, inhibits highly metastatic MDA-MB-231 breast cancer growth in vitro and in vivo by targeting the MDM2 oncogene

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