The inhibition of activated hepatic stellate cells proliferation by arctigenin through G0/G1 phase cell cycle arrest: Persistent p27Kip1 induction by interfering with PI3K/Akt/FOXO3a signaling pathway

Li, Ao; Wang, Jun; Wu, Mei‐Hwan; Zhang, Xiaoxun; Zhang, Hongzhi

doi:10.1016/j.ejphar.2014.11.040

Cited by 65 publications

(37 citation statements)

References 52 publications

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“…Relevant studies have revealed that P27 is also associated with liver fibrosis. The activation of P27 could induce HSCs cell cycle arrest, leading to the inhibition of HSCs growth and the reduction of expression levels of pro-fibrogenic genes 38 . In present studies, our data also shows that P27 is obviously up-regulated in Sjp40-treated group and over-expression of SKP2 could down-regulate P27 level.…”

Section: Discussionmentioning

confidence: 99%

Egg antigen p40 of Schistosoma japonicum promotes senescence in activated hepatic stellate cells via SKP2/P27 signaling pathway

Chen

Zhu

et al. 2017

Sci Rep

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Schistosomiasis is characterized by egg deposition, granulomatous inflammatory reaction and then subsequent hepatic fibrosis formation. Activated HSCs are regarded as the main effector cells in the progression of liver fibrosis and induction of senescence in hepatic stellate cells (HSCs) is vital to the reversion of hepatic fibrosis. Our previous work has showed that S. japonicum egg antigen p40 (Sjp40) could promote HSCs senescence via a STAT3/p53/p21 mechanism. In this paper, the major aim was to explore whether there are other signaling pathways in the process of Sjp40-induced HSCs aging and the underlying effect of SKP2/P27 signal pathway in this procedure. We observed the Sjp40-induced decrease of α-SMA and the senescence of LX-2 cells, and Sjp40 could upregulate P27 and downregulate the protein level of SKP2. The senescence induced by Sjp40 might be reversed in LX-2 cells that treated with P27-specific siRNA or with SKP2-special over-expression plasmid. In addition, we also demonstrated that the decreased expression of P-Rb and α-SMA induced by Sjp40 were partly restored by SKP2-overexpression. These data suggest that Sjp40 might inhibit HSCs activation by promoting cellular senescence via SKP2/P27 signaling pathway, which put forward novel mechanism in the treatment of liver fibrosis.

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Section: Discussionmentioning

confidence: 99%

Egg antigen p40 of Schistosoma japonicum promotes senescence in activated hepatic stellate cells via SKP2/P27 signaling pathway

Chen

Zhu

et al. 2017

Sci Rep

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“…Reduced levels of p27 have been linked with poor prognosis in tumor patients (47). Li et al (48) reported that p27 silencing significantly attenuates the suppressive effect of arctigenin on the proliferation of HSCs. In this study, our results revealed that decreased cell activation and proliferation by GAS5 overexpression were partially rescued by miR-222 mimics, p27 siRNA1, or p27 siRNA1 in combination with miR-222 mimics.…”

Section: Discussionmentioning

confidence: 99%

Long Non-coding RNA Growth Arrest-specific Transcript 5 (GAS5) Inhibits Liver Fibrogenesis through a Mechanism of Competing Endogenous RNA

Zheng²,

Mao

et al. 2015

Journal of Biological Chemistry

134

104

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“…[1][2][3][4][5][6] Recently, Li et al reported that Arctigenin exhibited neuroprotective activity via reducing surplus ROS production and downregulated the mitochondrial membrane potential. [11][12][13][14][15][16][17][18][19][20][21][22] However, to our knowledge, inhibition mechanism of Arctigenin on the metastasis, invasion and angiogenesis of tumor cells have not been studied detailed. 8 Moreover, the Arctigenin induced mitochondrial caspase-independent apoptosis of MDA-MB-231 cells through regulation of the NOX1 and p38-MAPK pathway.…”

Section: Introductionmentioning

confidence: 99%

Integrated in silico and experimental methods revealed that Arctigenin inhibited angiogenesis and HCT116 cell migration and invasion through regulating the H1F4A and Wnt/β-catenin pathway

Zhang

Song

et al. 2015

Mol. BioSyst.

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Arctigenin (ARG) has been previously reported to exert diverse biological activities including anti-proliferation, anti-inflammatory, and antiviral, etc. In the current study, the anti-metastasis and anti-angiogenesis activities of ARG were investigated. To further understand how ARG played these bioactivities, proteomic approaches were used to profile the proteome changes in response to ARG treatment using 2DE-MS/MS. Using these approaches, a total of 50 differentially expressed proteins were identified and clustered. Bioinformatics analysis suggested that multiple signalling pathways were involved. Moreover, ARG induced anti-metastatic and anti-angiogenesis activities were mainly accompanied by a deactivation of the Wnt/β-catenin pathway in HCT116 cells.

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The inhibition of activated hepatic stellate cells proliferation by arctigenin through G0/G1 phase cell cycle arrest: Persistent p27Kip1 induction by interfering with PI3K/Akt/FOXO3a signaling pathway

Cited by 65 publications

References 52 publications

Egg antigen p40 of Schistosoma japonicum promotes senescence in activated hepatic stellate cells via SKP2/P27 signaling pathway

Egg antigen p40 of Schistosoma japonicum promotes senescence in activated hepatic stellate cells via SKP2/P27 signaling pathway

Long Non-coding RNA Growth Arrest-specific Transcript 5 (GAS5) Inhibits Liver Fibrogenesis through a Mechanism of Competing Endogenous RNA

Integrated in silico and experimental methods revealed that Arctigenin inhibited angiogenesis and HCT116 cell migration and invasion through regulating the H1F4A and Wnt/β-catenin pathway

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