Oxymatrine induces nasopharyngeal cancer cell death through inhibition of PI3K/AKT and NF-κB pathways

Ni, Zhili; Yi, Jingmei

doi:10.3892/mmr.2017.7822

Cited by 17 publications

(13 citation statements)

References 26 publications

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“…These results showed that the inhibition effect of oxymatrine on migration and invasion in MHCC97H cells was not due to cytotoxicity. The results are similar with previous studies among those oxymatrine could inhibit the invasion of various cancers, including glioblastoma, colorectal cancer, gallbladder cancer cells, gastric cancer and osteosarcoma [15][16][17][18][19][20][21].…”

Section: Discussionsupporting

confidence: 92%

Oxymatrine inhibits the migration and invasion of hepatocellular carcinoma cells by reducing the activity of MMP-2/-9 via regulating p38 signaling pathway

Chen¹,

Zhu²,

Ye³

et al. 2019

J. Cancer

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As one of the major alkaloid components in Sophoraflavescensait (kushen), oxymatrine has been used widely across the world in anti-inflammatory and anti-cancer therapies. However, the effect in the metastasis of hepatocellular carcinoma (HCC) and related mechanism(s) are still unclear. The present study aimed to investigate the anti-metastatic effect of oxymatrine on HCC cells. Oxymatrine could also inhibit the protein levels of MMP-2/-9 in a dose-dependent relationship. Moreover, oxymatrine reduces the activity of p38 signaling pathway via inhibiting the phosphorylation of p38. The inhibition effect of oxymatrine on the expression of MMP-2/-9 and the phosphorylated of p38 was also detected in vivo. Combined treatment with p38 signaling pathway inhibitor and oxymatrine may have a synergistic effect on MMP-2/-9 and invasion of HCC cells. Therefore, oxymatrine may have inhibited GBC invasiveness by reducing the expression of MMP-2/-9 via inhibiting the activity of p38 signaling pathway. As a potentially novel therapeutic drug, oxymatrine may play an important role in the treatment of HCC.

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Section: Discussionsupporting

confidence: 92%

Oxymatrine inhibits the migration and invasion of hepatocellular carcinoma cells by reducing the activity of MMP-2/-9 via regulating p38 signaling pathway

Chen¹,

Zhu²,

Ye³

et al. 2019

J. Cancer

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“…Previous studies have suggested that the PI3K/Akt signaling pathway is involved in the apoptosis of various tumor cells ( 41 , 42 ). Furthermore, it has been revealed that certain drugs could decrease apoptosis and oxidative stress of cells via regulation of the PI3K/Akt signaling pathway ( 41 , 43 , 44 ). Numerous drugs and proteins exert potential protective effects on myocardial injury via regulation of the PI3K/Akt signaling pathway ( 45 – 47 ).…”

Section: Discussionmentioning

confidence: 99%

The protective effects of total paeony glycoside on ischemia/reperfusion injury in H9C2 cells via inhibition of the PI3K/Akt signaling pathway

2018

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At present, cardiovascular disease is the global leading cause of mortality. Total paeony glycoside (TPG) is a traditional Chinese medicine, which serves a pivotal role in the cardiovascular system. In the present study, the effects and underlying mechanisms of TPG on ischemia/reperfusion (I/R) injury-induced apoptosis of cardiomyocytes were investigated in vitro. Cell Counting kit-8 and flow cytometry were used to assess the viability, reactive oxygen species (ROS) content and apoptosis of H9C2 cells. The activities of lactate dehydrogenase (LDH), malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GPX) were analyzed by commercial detection kits. Reverse transcription-quantitative polymerase chain reaction and western blot analysis were conducted to evaluate the expression levels of various factors. The results demonstrated that the viability of H9C2 cells was not significantly altered in response to various concentrations of TPG. However, following I/R injury, TPG markedly enhanced cell viability in a time- and dose-dependent manner. Furthermore, TPG decreased the rate of apoptosis and ROS levels, and reduced the activities of MDA and LDH. Conversely, TPG increased SOD and GPX activities. In addition, TPG upregulated the expression levels of pro-caspase-3 and B-cell lymphoma2 (Bcl-2), whereas it downregulated cleaved-caspase-3, poly (ADP-ribose) polymerase 1, Bcl-2-associated X protein, phosphorylated (p)-phosphatidylinositol 3 kinase (PI3K) and p-protein kinase B (Akt) expression. Treatment with insulin-like growth factor-1 increased the apoptosis of H9C2 cells, thus suggesting that activation of the PI3K/Akt signaling pathway reversed the protective effects of TPG. Taken together, TPG may suppress I/R-induced apoptosis and oxidative stress of H9C2 cells possibly by inhibiting the PI3K/Akt signaling pathway; such a phenomenon may have a therapeutic effect on cardiovascular disease.

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“…Ni et al reported that MDR of nasopharyngeal carcinoma (NPC) was reversed by inhibition of the PI3K/AKT/NF-κB signaling pathway. It primarily promoted the expression of p53 and Bax protein in NPC HK-1 cells via regulation of the PI3K/AKT/NF-κB pathway and inhibited the expression of cyclin D protein 69 . NF-κB promotes cells to pass the G1/S checkpoint by stimulating transcription of cyclin D1, which accelerates cell progression, promotes tumor growth, and leads to drug resistance 24 .…”

Section: Pi3k/akt/nf-κbmentioning

confidence: 97%

PI3K/AKT pathway as a key link modulates the multidrug resistance of cancers

et al. 2020

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Multidrug resistance (MDR) is the dominant challenge in the failure of chemotherapy in cancers. Phosphatidylinositol 3-kinase (PI3K) is a lipid kinase that spreads intracellular signal cascades and regulates a variety of cellular processes. PI3Ks are considered significant causes of chemoresistance in cancer therapy. Protein kinase B (AKT) is also a significant downstream effecter of PI3K signaling, and it modulates several pathways, including inhibition of apoptosis, stimulation of cell growth, and modulation of cellular metabolism. This review highlights the aberrant activation of PI3K/AKT as a key link that modulates MDR. We summarize the regulation of numerous major targets correlated with the PI3K/AKT pathway, which is further related to MDR, including the expression of apoptosis-related protein, ABC transport and glycogen synthase kinase-3 beta (GSK-3β), synergism with nuclear factor kappa beta (NF-κB) and mammalian target of rapamycin (mTOR), and the regulation of glycolysis.

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Oxymatrine induces nasopharyngeal cancer cell death through inhibition of PI3K/AKT and NF-κB pathways

Cited by 17 publications

References 26 publications

Oxymatrine inhibits the migration and invasion of hepatocellular carcinoma cells by reducing the activity of MMP-2/-9 via regulating p38 signaling pathway

Oxymatrine inhibits the migration and invasion of hepatocellular carcinoma cells by reducing the activity of MMP-2/-9 via regulating p38 signaling pathway

The protective effects of total paeony glycoside on ischemia/reperfusion injury in H9C2 cells via inhibition of the PI3K/Akt signaling pathway

PI3K/AKT pathway as a key link modulates the multidrug resistance of cancers

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