Paeoniflorin modulates multidrug resistance of a human gastric cancer cell line via the inhibition of NF-κB activation

Liu, Ping

doi:10.3892/mmr.2011.652

Cited by 21 publications

(16 citation statements)

References 31 publications

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“…It has been reported that the extracts like peoniflorin, curcumin and procyanidin etc. could effectively inhibit the activity of NF-κB, down-regulate the expression of ABCB1 and decrease the P-gp expression 19-23. In our works, we have employed the extract of Traditional Chinese Medicine Stemona japonica, tuberostemonine as the MDR reversal agent, to study its reversal effect on myelogenous leukemia adriamycin-resistance cells K562/ADR.…”

Section: Discussionmentioning

confidence: 99%

Tuberostemonine reverses multidrug resistance in chronic myelogenous leukemia cells K562/ADR

Wang

Zhu

et al. 2017

J. Cancer

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Objective: To investigate the reversal effect of tuberostemonine on MDR in myelogenous leukemia cells K562/ADR.Methods: Human myelogenous leukemia cells K562 and their adriamycin-resistance cells K562/ADR were used. The growth curve of cells treated by tuberostemonine and the Non-toxic concentration of tuberostemonine were determined by MTT, Cell apoptosis was determined by MTT and flow cytometry. The expression of MDR1, Survivin and Livin was detected by RT-PCR. The activity of P-gp was detected by flow cytometry. Western blot was used to detect the expression of NF-κB and Survivin.Results: The effect of tuberostemonine on K562/ADR showed a dose-dependence, and 350μg/mL and 500μg/mL of tuberostemonine could inhibit the expression of MDR1 (P<0.05). While no function difference of P-gp was detected. With the increased concentration of tuberostemonine, the inhibitory effect were enhanced to the expression of NF-κB. Tuberostemonine combined with adriamycin could time-dependently inhibit the cell proliferation (P<0.05) and obviously promoted the cell apoptosis (P<0.05). Also the tuberostemonine could inhibit the expression of Survivin.Conclusion: There are no direct relations between tuberostemonine and P-gp, but tuberostemonine could reverse the multidrug resistance of K562/ADR via down-regulating the expression of Nf-κB and inhibiting th1e expression of Survivin.

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Section: Discussionmentioning

confidence: 99%

Tuberostemonine reverses multidrug resistance in chronic myelogenous leukemia cells K562/ADR

Wang

Zhu

et al. 2017

J. Cancer

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“…PF, the principal component of Total glucosides of paeonia (TGP), has also been shown to exert anti-cancer and anti-proliferative activity in cultured cells as well as in animal models. Previous studies have shown that PF induces cancer cell apoptosis in gastric cancer cells, liver cancer cells, ovarian cancer cells and leukemia cells through various mechanisms, such as the modulation of the NF-kB activation pathway, Bcl-2 and Bax expression, or the MDM2-p53 pathway 32 33 34 35 36 37 38 . In these published reports, the PF concentrations were prescribed at a milligram level, which limits its use in the clinical setting.…”

Section: Discussionmentioning

confidence: 99%

Paeoniflorin Potentiates the Inhibitory Effects of Erlotinib in Pancreatic Cancer Cell Lines by Reducing ErbB3 Phosphorylation

Hao

Yang

Ding

et al. 2016

Sci Rep

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Blockade of the epidermal growth factor receptor (EGFR) by EGFR tyrosine kinase inhibitors is insufficient for effective anti-tumor activity because the reactivation of the ErbB3 signaling pathway significantly contributes to activating the consequent phosphoinositide 3-kinase (PI3K)/Akt signaling pathway. Combinatorial therapies including ErbB3 targeting may ameliorate tumor responses to anti-EGFR therapies. In the present study, we found that in BxPC-3 and L3.6pl cells, which highly expressed the ErbB3 receptor, significant reduction in cell viability, induction of apoptosis were observed when treated with a combination of erlotinib and PF compared to either agent alone. Moreover, in ErbB3-expressing BxPC-3, L3.6pl and S2VP10 cell lines, the inhibition of ErbB3/PI3K/Akt phosphorylation were observed when treated with PF. Most strikingly, both EGFR/MAPK/Erk and ErbB3/PI3K/Akt activitions were substantially suppressed when treated with the combination of PF and erlotinib. However, in the ErbB3-deficient cell line MIAPaCa-2, no such effects were observed with similar treatments. Most importantly, these in vitro results were replicated in nude mouse transplanted tumor models. Taken together, our findings show that PF enhances the effect of erlotinib in ErbB3-expressing pancreatic cancer cells by directly suppressing ErbB3 activation, and PF in combination with erlotinib is much more effective as an antitumor agent compared with either agent alone.

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“…In the in vivo study, we observed that oral administration of Pae significantly inhibited tumour growth and that Pae & Cis showed synergistically inhibitory effects on the growth of tumours. Some (19) concluded that Pae at non-toxic concentrations effectively modulated multidrug resistance of a human gastric cancer cell line via inhibition of nuclear factor-kappa B activation. Similarly, Hao et al (12) previously confirmed that Pae enhanced the effect of erlotinib in pancreatic cancer cells by directly suppressing human epidermal growth factor receptor-3 activation.…”

Section: Resultsmentioning

confidence: 99%

Paeoniflorin inhibits the growth of bladder carcinoma via deactivation of STAT3

et al. 2018

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Bladder cancer (BCa) is one of the most common urinary cancers. The present study aims to investigate whether Paeoniflorin (Pae) can exert inhibitory effects on BCa. The results showed that Pae inhibited proliferation of human BCa cell lines in a concentration- and time-dependent manner. Pae and cisplatin (Cis) synergistically inhibited the growth of tumours in RT4-bearing mice. Pae treatment neutralized the body loss induced by Cis. Moreover, Pae induced apoptosis in RT4 cells and increased the activities of caspase3, caspase8 and caspase9. Western blotting and immunohistochemical analysis revealed that the phosphorylated signal transducer and activator of transcription-3 (p-STAT3) level were decreased in Pae-treated RT4 cells and Pae-treated tumour-bearing mice. Furthermore, STAT3 transcriptional target B-cell lymphoma-2 was decreased in Pae-treated RT4 cells. Interestingly, Pae prevented translocation of STAT3 to the nucleus in RT4 cells. Collectively, Pae inhibits the growth of BCa, at least in part, via a STAT3 pathway.

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Paeoniflorin modulates multidrug resistance of a human gastric cancer cell line via the inhibition of NF-κB activation

Cited by 21 publications

References 31 publications

Tuberostemonine reverses multidrug resistance in chronic myelogenous leukemia cells K562/ADR

Tuberostemonine reverses multidrug resistance in chronic myelogenous leukemia cells K562/ADR

Paeoniflorin Potentiates the Inhibitory Effects of Erlotinib in Pancreatic Cancer Cell Lines by Reducing ErbB3 Phosphorylation

Paeoniflorin inhibits the growth of bladder carcinoma via deactivation of STAT3

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