Paeoniflorin inhibits human glioma cells via STAT3 degradation by the ubiquitin&amp;ndash;proteasome pathway

Nie, Xiaohu; Ouyang, Jia; Xing, Ying; Li, Danyan; Dong, Xing-Yu; Liu, Ruen; Xu, Ran

doi:10.2147/dddt.s93912

Cited by 27 publications

(14 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As expected, we also found that Pae inhibited translocation of STAT3 to the nucleus in RT4 cells. It is noteworthy that a recent study conducted by Nie et al (13) found rapid down-regulation of STAT3 that was consistent with its accelerated degradation, and the pro-degradation effect of Pae on STAT3 was mainly through the ubiquitin-proteasome pathway. Therefore, these findings clearly indicate that deactivation of STAT3 by Pae contributes to its inhibitory effects on BCa development.…”

Section: Resultssupporting

confidence: 58%

“…Pae, extracted from RPA, is a natural anti-cancer medicine. Many pharmacological studies have reported that Pae exerts anti-cancer and anti-proliferative activity in cultured tumour cells, as well as in tumour xenograft models (12)(13)(14)(15). In 2016, Lin et al (16) reported the anti-proliferative properties of RPA extract on BCa, both in vitro and in vivo.…”

Section: Resultsmentioning

confidence: 99%

“…Today, there is interest in studying the therapeutic effects of Pae on different cancer types. In previous pharmacological investigations, Pae was confirmed to inhibit the growth of human pancreatic cancer, gastric carcinoma cells, colorectal carcinoma cells, and glioma cells (12)(13)(14)(15). A new study (16) recently reported the anti-proliferative properties of RPA extraction in treating BCa, both in vitro and in vivo.…”

mentioning

confidence: 91%

See 2 more Smart Citations

Paeoniflorin inhibits the growth of bladder carcinoma via deactivation of STAT3

et al. 2018

View full text Add to dashboard Cite

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.

show abstract

Section: Resultssupporting

confidence: 58%

Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 91%

See 1 more Smart Citation

Paeoniflorin inhibits the growth of bladder carcinoma via deactivation of STAT3

et al. 2018

View full text Add to dashboard Cite

show abstract

“…The pool of STAT3 in cells is submitted to a fine regulation consisting in several mechanisms. This includes a synthesis-degradation cycle, controlled by proteasomedependent pathways, that regulates total STAT3 availability [60,61]. Another mechanism is an activation-inactivation cycle that makes STAT3 activation transient as a rule.…”

Section: General Description Of Stat3 Pathway Signallingmentioning

confidence: 99%

Role of STAT3 in Genesis and Progression of Human Malignant Gliomas

et al. 2016

View full text Add to dashboard Cite

Signal transducer and activator of transcription 3 (STAT3) is aberrantly activated in glioblastoma and has been identified as a relevant therapeutic target in this disease and many other human cancers. After two decades of intensive research, there is not yet any approved STAT3-based glioma therapy. In addition to the canonical activation by tyrosine 705 phosphorylation, concordant reports described a potential therapeutic relevance of other post-translational modifications including mainly serine 727 phosphorylation. Such reports reinforce the need to refine the strategy of targeting STAT3 in each concerned disease. This review focuses on the role of serine 727 and tyrosine 705 phosphorylation of STAT3 in glioma. It explores their contribution to glial cell transformation and to the mechanisms that make glioma escape to both immune control and standard treatment.

show abstract

“…Paeoniflorin (PAE) is a principal bioactive component of the root of Paeonia lactiflora Pall., a medicinal herb species found in Korea, Japan and China ( 10 ). In Traditional Chinese Medicine, PAE has been widely used ( 11 ). It has been reported that PAE exerts numerous pharmacological effects, such as anti-inflammatory ( 12 , 13 ), anti-allergy ( 14 , 15 ), immunoregulatory ( 16 , 17 ), neuroprotective ( 18 ) and hepatoprotective effects ( 19 ).…”

Section: Introductionmentioning

confidence: 99%

Paeoniflorin inhibits proliferation of endometrial cancer cells via activating MAPK and NF‑κB signaling pathways

Zhang

Wang

et al. 2017

Exp Ther Med

View full text Add to dashboard Cite

Paeoniflorin (PAE), a principal bioactive component of Paeonia lactiflora Pall., appears to have antitumor properties. However, the pharmacological activity of PAE in endometrial cancer and the specific mechanisms have remained largely elusive. The present study aimed to determine the antitumor activity of PAE in the human endometrial cancer cell line RL95-2 and explore the potential mechanisms. Cell proliferation was assessed to evaluate the antitumor effect of PAE towards RL95-2 cells via a Cell Counting Kit-8 assay. Protein expression was examined to investigate changes in the signaling pathways of p38 mitogen-activated protein kinase (MAPK), c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase (ERK) and nuclear factor (NF)-κB in RL95-2 cells during PAE treatment by western blot analysis. The results revealed that PAE significantly and dose- and time-dependently inhibited the proliferation of RL95-2 cells. In addition, PAE activated MAPK signaling pathways (p38, JNK and ERK) and the NF-κB signaling pathway. Furthermore, p38 MAPK and NF-κB inhibitors (SB203580 and MG-132, respectively) prevented PAE-induced proliferative inhibition in RL95-2 cells. However, ERK and JNK inhibitors (PD98059 and BI-78D3, respectively) did not produce such an inhibition. In conclusion, the present study demonstrated that PAE exerts its anti-proliferative activity via activating p38 MAPK and NF-κB signaling pathways in endometrial cancer cells, providing a potential new drug of choice for endometrial cancer therapy.

show abstract

Paeoniflorin inhibits human glioma cells via STAT3 degradation by the ubiquitin–proteasome pathway

Cited by 27 publications

References 44 publications

Paeoniflorin inhibits the growth of bladder carcinoma via deactivation of STAT3

Paeoniflorin inhibits the growth of bladder carcinoma via deactivation of STAT3

Role of STAT3 in Genesis and Progression of Human Malignant Gliomas

Paeoniflorin inhibits proliferation of endometrial cancer cells via activating MAPK and NF‑κB signaling pathways

Contact Info

Product

Resources

About