Oroxylin a prevents inflammation‐related tumor through down‐regulation of inflammatory gene expression by inhibiting NF‐κB signaling

Yao, Jing; Hu, Rong; Sun, Jie; Lin, Biqi; Zhao, Li; Sha, Yunying; Zhu, Binbin; Qin, You; Yan, Tianhua; Guo, Qinglong

doi:10.1002/mc.21958

Cited by 51 publications

(42 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…From one side it has been demonstrated that a great promotion to the malignancy can come from gene adaptation to the hypoxia (Shay and Celeste Simon, 2012). From the other side it has been shown that many proinflammatory genes are overexpressed by malignant cells (Tafani et al, 2011a,b; Jin et al, 2012; Schito et al, 2012; Yao et al, 2012; De Santis et al, 2013). Bridging hypoxia adaptation and proinflammatory gene expression by cancer cells, we suggested the hypothesis that these two very complex cell responses, when sequentially activated, could be a good candidate framework to explain all the properties of the malignant phenotype.…”

Section: Introduction: a New Paradigm On Cancer Pathogenesismentioning

confidence: 99%

Modulators of HIF1α and NFkB in Cancer Treatment: Is it a Rational Approach for Controlling Malignant Progression?

Tafani¹,

Pucci²,

Russo³

et al. 2013

Front. Pharmacol.

View full text Add to dashboard Cite

HIF1α and NFkB are two transcription factors very frequently activated in tumors and involved in tumor growth, progression, and resistance to chemotherapy. In fact, HIF1α and NFkB together regulate transcription of over a thousand genes that, in turn, control vital cellular processes such as adaptation to the hypoxia, metabolic reprograming, inflammatory reparative response, extracellular matrix digestion, migration and invasion, adhesion, etc. Because of this wide involvement they could control in an integrated manner the origin of the malignant phenotype. Interestingly, hypoxia and inflammation have been sequentially bridged in tumors by the discovery that alarmin receptors genes such as RAGE, P2X7, and some TLRs, are activated by HIF1α; and that, in turn, alarmin receptors strongly activate NFkB and proinflammatory gene expression, evidencing all the hallmarks of the malignant phenotype. Recently, a large number of drugs have been identified that inhibit one or both transcription factors with promising results in terms of controlling tumor progression. In addition, many of these molecules are natural compounds or off-label drugs already used to cure other pathologies. Some of them are undergoing clinical trials and soon they will be used alone or in combination with standard anti-tumoral agents to achieve a better treatment of tumors with reduction of metastasis formation and, more importantly, with a net increase in survival. This review highlights the central role of HIF1α activated in hypoxic regions of the tumor, of NFkB activation and proinflammatory gene expression in transformed cells to understand their progression toward malignancy. Different molecules and strategies to inhibit these transcription factors will be reviewed. Finally, the central role of a new class of deacetylases called Sirtuins in regulating HIF1α and NFkB activity will be outlined.

show abstract

Section: Introduction: a New Paradigm On Cancer Pathogenesismentioning

confidence: 99%

Modulators of HIF1α and NFkB in Cancer Treatment: Is it a Rational Approach for Controlling Malignant Progression?

Tafani¹,

Pucci²,

Russo³

et al. 2013

Front. Pharmacol.

View full text Add to dashboard Cite

show abstract

“…To elucidate the observed results, we hypothesized that beta-adrenergic receptors activation shall exert a suppressive effect on NF-κβ and its inhibitor IκBα as it is well documented that NF-κB plays a key role in modulating the gene expression [37,38]. Phosphorylation of NF-κB p65 at Ser-536 was markedly reduced after beta-adrenergic receptor stimulation.…”

Section: Discussionmentioning

confidence: 99%

Beta Adrenergic Receptors Stimulation Attenuates Phosphorylation of NF-κB and IκBα in Hyperglycemic Endothelial Cells

Safi

Shah

Qvist

et al. 2018

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: NF-κB induces transcription of a number of genes, associated with inflammation and apoptosis. In this study, we have investigated the effect of β-adrenergic receptor stimulation on NF-κB and IκBα in HUVECs. Methods: Human umbilical vein endothelial cells (HUVECs) were cultured in high and low glucose concentrations. All HUVECs were treated with different concentrations of isoproterenol and propranolol for different time periods. The analytical procedures consisted of Western Blot, ELISA, DCFH-DA and TUNEL assays. Results: Isoproterenol (agonist of a beta-adrenergic receptor) significantly reduced phosphorylation at Ser-536 of NF-κB; and Ser-32 and Ser-36 of IκBα in hyperglycemic HUVECs. Isoproterenol also significantly reduced apoptosis and ROS generation. No effect of IκBα was observed on Tyr-42 phosphorylation. The effect of isoproterenol was reversed by the antagonist propranolol. We also checked if NF-κB inhibitor MG132 causes any change at the level of apoptosis. However, we observed an almost similar effect. Conclusion: Given data demonstrates that beta-adrenergic receptors stimulation has a protective effect on HUVECs that might be occuring via NF-κβ and IκBα pathway.

show abstract

“…Nuclear and cytosolic protein extracts were prepared according to the modified method as described previously [50]. The cytosolic and nuclear fractions was subjected to immunoblot analysis.…”

Section: Methodsmentioning

confidence: 99%

“…The cytosolic, nuclear extracts and whole cell lysates were prepared and subjected to Western blot analysis as described previously [50]. Bands were detected immunologically using antibodies against PI3K (1:800), Akt (1:800), p-Akt (1:800), IKKα (1:800), p-IKKα (1:800), p-IκBα (1:800), Cyclin D1 (1:800), survivin (1:800) NF-κB (1:500), phospho-p65 (1:500).…”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Wogonoside prevents colitis-associated colorectal carcinogenesis and colon cancer progression in inflammation-related microenvironment via inhibiting NF-κB activation through PI3K/Akt pathway

et al. 2016

Self Cite

View full text Add to dashboard Cite

The inflammatory microenvironment has been reported to be correlated with tumor initiation and malignant development. In the previous studies we have found that wogonoside exerts anti-neoplastic and anti-inflammatory activities. In this study, we aimed to further investigate the chemopreventive effects of wogonoside on colitis-associated cancer and delineated the potential mechanisms. In the azoxymethane initiated and dextran sulfate sodium (AOM/DSS) promoted colorectal carcinogenesis mouse model, wogonoside significantly reduced the disease severity, lowered tumor incidence and inhibited the development of colorectal adenomas. Moreover, wogonoside inhibited inflammatory cells infiltration and cancer cell proliferation at tumor site. Furthermore, wogonoside dramatically decreased the secretion and expression of IL-1β, IL-6 and TNF-α as well as the nuclear expression of NF-κB in adenomas and surrounding tissues. In vitro results showed that wogonoside suppressed the proliferation of human colon cancer cells in the inflammatory microenvironment. Mechanistically, we found that wogonoside inhibited NF-κB activation via PI3K/Akt pathway. In conclusion, our results demonstrated that wogonoside attenuated colitis-associated tumorigenesis in mice and inhibited the progression of human colon cancer in inflammation-related microenvironment via suppressing NF-κB activation by PI3K/Akt pathway, indicating that wogonoside could be a promising therapeutic agent for colorectal cancer.

show abstract

Oroxylin a prevents inflammation‐related tumor through down‐regulation of inflammatory gene expression by inhibiting NF‐κB signaling

Cited by 51 publications

References 46 publications

Modulators of HIF1α and NFkB in Cancer Treatment: Is it a Rational Approach for Controlling Malignant Progression?

Modulators of HIF1α and NFkB in Cancer Treatment: Is it a Rational Approach for Controlling Malignant Progression?

Beta Adrenergic Receptors Stimulation Attenuates Phosphorylation of NF-κB and IκBα in Hyperglycemic Endothelial Cells

Wogonoside prevents colitis-associated colorectal carcinogenesis and colon cancer progression in inflammation-related microenvironment via inhibiting NF-κB activation through PI3K/Akt pathway

Contact Info

Product

Resources

About