Combination of ginsenoside Rg3 with docetaxel enhances the susceptibility of prostate cancer cells via inhibition of NF-κB

Kim, Sun Mi; Lee, So Yong; Cho, Jin Suk; Son, Seung Mo; Choi, Sang Sook; Yun, Yong Soo; Yoo, Hyun-jung; Yoon, Do Young; Oh, Ki‐Wan; Han, Sang Bae; Hong, Jin Tae

doi:10.1016/j.ejphar.2009.12.018

Cited by 130 publications

(89 citation statements)

References 50 publications

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“…Kim et al reported that for prostate cancer, ginsenoside Rg3 enhanced the chemosensitivity of prostate cancer cells for docetaxel by the inhibition of NF-κB (16). They also demonstrated that the combined treatment of ginsenoside Rg3 with cisplatin inhibited the growth of prostate cancer cells more than either of the single regimen treatments.…”

Section: Discussionmentioning

confidence: 89%

Synergistic antitumor effect of ginsenoside Rg3 and cisplatin in cisplatin-resistant bladder tumor cell line

LEE¹,

LEE²,

Ho³

et al. 2014

Oncology Reports

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Abstract. Cisplatin-based chemotherapy is the first-line treatment for metastatic urothelial cell carcinoma. However, for cisplatin-resistant cases, no chemotherapeutic agent has been established as a standard of treatment. This study aimed to investigate the synergistic antitumor effect of ginsenoside Rg3 on cisplatin in cisplatin-resistant bladder cancer cells (T24R2). T24R2 cells were treated with cisplatin and/or ginsenoside Rg3. Cell viability was assessed by the Cell Counting Kit-8 and clonogenic assays. Synergism between ginsenoside Rg3 and cisplatin was determined when the combination index was <1.0. Flow cytometry was used to evaluate the cell cycle distribution. To estimate the changes of proteins associated with the cell cycle and apoptosis following the treatment of ginsenoside Rg3, western blotting and densitometric assays were performed for caspase-3, -8 and -9, cyclin B1, Bcl-2, Bad, p21 and cytochrome c. The Cell Counting Kit-8 and clonogenic assays showed the synergistic antitumor effect of ginsenoside Rg3 on cisplatin, while the combination index was <1.0, confirming the synergism. Cell cycle alterations at the G2/M phase caused by cisplatin were greater after the combination with ginsenoside Rg3. Western blotting and densitometric assay showed that the expression of Bcl-2 was decreased after the combined treatment of ginsenoside Rg3 and cisplatin, whereas the expression of cytochrome c and caspase-3 were increased, suggesting the activation of the intrinsic apoptotic pathway. In conclusion, ginsenoside Rg3 inhibited the proliferation of cisplatin-resistant bladder cancer cells in a synergistic manner with cisplatin. Activation of the intrinsic apoptotic pathway and the enhancement of cell cycle alterations are possible explanations for this result.

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Section: Discussionmentioning

confidence: 89%

Synergistic antitumor effect of ginsenoside Rg3 and cisplatin in cisplatin-resistant bladder tumor cell line

LEE¹,

LEE²,

Ho³

et al. 2014

Oncology Reports

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show abstract

“…Pan et al (21) reported that ginsenoside Rg3 attenuates cell migration via inhibition of aquaporin 1 expression in PC-3M prostate cancer cells. Furthermore, Kim et al (22) confirmed that the combination of ginsenoside Rg3 with docetaxel enhanced the susceptibility of prostate cancer cells via inhibition of NF-κB. However, it had not been elucidated whether ginsenoside Rg3 combined with paclitaxel and cisplatin enhances their inhibitory effects on the Eca-109 xenograft in mice.…”

Section: Discussionmentioning

confidence: 84%

Ginsenoside Rg3 enhances the inhibitory effects of chemotherapy on esophageal squamous cell carcinoma in mice

Chang

Huo

et al. 2014

Molecular and Clinical Oncology

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Abstract. The present study was conducted in order to investigate the inhibitory effects of ginsenoside Rg3 combined with chemotherapy on Eca-109 esophageal squamous cell carcinoma (ESCC) in mice. Tumor xenograft models were established in the right forelimb of 20 BALB/c nude mice by subcutaneous injection. The tumor-bearing mice were randomly assigned to 4 treatment groups (n=5 per group) as follows: the control group (saline), the ginsenoside Rg3 alone group (6 mg/kg/day, once a day for 3 weeks), the chemotherapy alone group (paclitaxel 10 mg/kg/day + cisplatin 5 mg/kg/day on days 1, 7, 14 and 21) and the chemotherapy + Rg3 group (combined treatment). The length and width of the tumor were directly measured with calipers at different time points and the tumor volume (cm 3 ) was calculated using the formula 0.52 x length x width 2 every other day. The mice were sacrificed by cervical dislocation following completion of therapy, the tumors were removed and weighed and the expression levels of Ki-67 were determined by immunohistochemistry. The results indicated that the coadministration of ginsenoside Rg3 significantly enhanced the inhibitory effects of chemotherapy on tumor growth. In addition, the expression levels of Ki-67 in the chemotherapy + Rg3 group were significantly lower compared to those in the other 3 groups. The chemotherapy + Rg3 group also exhibited the lowest microvascular density among all four groups. These findings suggested that ginsenoside Rg3 may improve the antitumor efficacy of chemotherapy in Eca-109 ESCC in mice.

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“…Ginsenoside Rg3 has been reported to inhibit NF-κB, induce G 1 arrest and enhance susceptibility to docetaxel and other chemicals in prostate cancer cells (41). Furthermore, the ginsenoside Rd has been demonstrated to elevate intracellular glutathione levels by increasing γ-glutamyl cysteine ligase activation in rat hepatocyte H4IIE cells through NF-κB-DNA binding (42).…”

Section: Kip1mentioning

confidence: 99%

Dammarane-type triterpene ginsenoside-Rg18 inhibits human non-small cell lung cancer A549 cell proliferation via G1 phase arrest

et al. 2018

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Abstract.A previous study reported that a novel dammarane-type triterpene saponin, ginsenoside-Rg18, derived from the root of Panax ginseng, displayed hydroxyl radical scavenging, anti-bacterial and cytotoxic activities. However, the underlying molecular mechanisms of its anti-proliferative effect on non-small cell lung cancer (NSCLC) A549 cells remains unclear. In the present study, it was determined that Rg18 inhibited the proliferation of A549 cells with a half-maximal inhibitory concentration of 150 µM. Flow cytometry analysis indicated that cell cycle progression was blocked by Rg18 at G 1 phase in A549 cells, which was accompanied by downregulation of cyclin-dependent kinase 2 (CDK2), CDK4, CDK6, cyclin D1, cyclin D2, cyclin E and phosphorylated retinoblastoma protein expression at the protein level. In addition, the CDK inhibitors (CDKNs), CDKN1A and CDKN1B, were upregulated following Rg18 treatment. Furthermore, Rg18 treatment resulted in the intracellular accumulation of reactive oxygen species (ROS), and a dose-dependent inhibition of p38 mitogen activated protein kinase (p38), c-Jun N-terminal kinase (JNK) and nuclear factor-κB (NF-κB)/p65 phosphorylation. Taken together, Rg18-mediated G 1 phase arrest was closely associated with the generation of intracellular ROS, and p38, JNK and NF-κB/p65 inhibition in A549 human NSCLC cells.

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Combination of ginsenoside Rg3 with docetaxel enhances the susceptibility of prostate cancer cells via inhibition of NF-κB

Cited by 130 publications

References 50 publications

Synergistic antitumor effect of ginsenoside Rg3 and cisplatin in cisplatin-resistant bladder tumor cell line

Synergistic antitumor effect of ginsenoside Rg3 and cisplatin in cisplatin-resistant bladder tumor cell line

Ginsenoside Rg3 enhances the inhibitory effects of chemotherapy on esophageal squamous cell carcinoma in mice

Dammarane-type triterpene ginsenoside-Rg18 inhibits human non-small cell lung cancer A549 cell proliferation via G1 phase arrest

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