Green tea inhibits cycolooxygenase-2 in non-small cell lung cancer cells through the induction of Annexin-1

Lu, Qing-Yi; Jin, Yusheng; Mao, Jenny T.; Zhang, Zuo‐Feng; Heber, David; Dubinett, Steven M.; Rao, Jianyu

doi:10.1016/j.bbrc.2012.09.125

Cited by 23 publications

(16 citation statements)

References 26 publications

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“…Here, we found that GTP intake was also associated with these parameters, except for VEGF-A expression. GTP was previously found to inhibit tumor growth [ 35 ], angiogenesis, [ 36 ], and COX-2 [ 37 ] and HO-1 [ 38 ] expression under pathological conditions including malignancy.…”

Section: Discussionmentioning

confidence: 99%

Green Tea Polyphenol Induces Changes in Cancer-Related Factors in an Animal Model of Bladder Cancer

et al. 2017

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Green tea polyphenol (GTP) suppresses carcinogenesis and aggressiveness in many types of malignancies including bladder cancer. However, the mechanistic basis of these effects is not well understood. This was investigated in the present study using a mouse model of chemically induced bladder cancer. C3H/He mice (8 weeks old; n = 46) were treated with 0.05% N-butyl-N-(4-hydroxybutyl) nitrosamine (BBN) solution for 14–24 weeks. Mice in the BBN + GTP group (n = 47) were also treated with 0.5% GTP solution over the same period. Tumor cell proliferation and microvessel density were evaluated along with immunohistochemical analysis of human antigen (Hu)R, vascular endothelial growth factor (VEGF)-A, cyclooxygenase (COX)-2, and hemeoxygenase (HO)-1 expression. Cytoplasmic HuR expression in cancer cells was higher at 14 and 24 weeks in the BBN than in the control group and was associated with increased invasion of tumor cells in muscle. However, these effects were not observed in the BBN + GTP group. A multivariate analysis of GTP intake and cytoplasmic HuR expression revealed that GTP was independently associated with COX-2 and HO-1 expression, while cytoplasmic HuR expression was associated with COX-2 and VEGF-A levels. Expression of COX-2 and HO-1 was associated with cell proliferation and that of VEGF-A and HO-1 was associated with angiogenesis. Nuclear HuR expression was not associated with any parameters such as carcinogenesis, muscle invasion, and GTP intake. These results indicate that GTP intake can suppress tumor progression and malignant behavior in an animal model of bladder cancer. We also speculate that GTP directly and indirectly suppresses tumor cell proliferation and angiogenesis via HuR-related pathways in bladder cancer.

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Section: Discussionmentioning

confidence: 99%

Green Tea Polyphenol Induces Changes in Cancer-Related Factors in an Animal Model of Bladder Cancer

et al. 2017

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“…In contrast, silencing annexin A1 expression overturned the inhibitory effect of GTE on COX-2. These results suggest that GTE shows its effect through inducing annexin A1 expression, therefore targeting annexin A1 could be a promising mechanism in preventing lung cancer [98].…”

Section: Annexin-targeted Studiesmentioning

confidence: 77%

Annexin Proteins: Novel Promising Targets for Anticancer Drug Development

Bakar¹

2017

Unique Aspects of Anti-Cancer Drug Development

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Intracellular Ca 2+ signaling and Ca 2+ homeostasis have long been an important subject area of cell biology. Several intracellular Ca 2+ binding proteins have been demonstrated until now, and among these, annexins are characterized by their ability to interact with membrane phospholipids and they form an evolutionary conserved multigene family with the members being expressed throughout animal and plant kingdoms. Annexin proteins are defined by different structural and biochemical criteria, and this multigene family has several biological features. In certain clinical conditions, the alterations on the localization or expression levels of annexin proteins are considered as the causes of pathological results and/or sequelae of disease. So, annexin proteins are indirectly linked to severe human diseases such as cardiovascular disease and cancer. Since annexin proteins are known to play roles in cancer, the researches are focused on defining the clinical significance of certain annexin proteins in cancer development and by the way anticancer treatments in the last decades. This chapter presents detailed information about annexin proteins and the studies on anticancer drug development targeting certain annexins. The studies denominate that targeting of certain annexin proteins reduces tumorigenesis and therapeutic resistance. So, annexin proteins have growing importance for anticancer drug development.

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“…After Cmp17b treatment, the Ptgs2 expression is downregulated in the aorta, possibly underpinned by the anti-inflammatory effects of FPR agonists. Specifically, this effect of Cmpd17b may be independent of diabetes as it has been reported that upregulation of the endogenous FPR agonist, Annexin A1, reduces Ptgs2 expression in lung cancer cells [50]. Despite observing a greater functional contribution of prostanoids to endothelium-dependent relaxation in Cmpd17b-treated diabetic mice, a compensatory downregulation of mRNA for prostacyclin synthase (PTGIS) was observed, without affecting Ptgs1 expression.…”

Section: Discussionmentioning

confidence: 91%

The Novel Small-molecule Annexin-A1 Mimetic, Compound 17b, Elicits Vasoprotective Actions in Streptozotocin-induced Diabetic Mice

Marshall

Qin

Jelinic

et al. 2020

IJMS

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The formyl peptide receptor (FPR) family are a group of G-protein coupled receptors that play an important role in the regulation of inflammatory processes. It is well-established that activation of FPRs can have cardioprotective properties. Recently, more stable small-molecule FPR1/2 agonists have been described, including both Compound 17b (Cmpd17b) and Compound 43 (Cmpd43). Both agonists activate a range of signals downstream of FPR1/2 activation in human-engineered FPR-expressing cells, including ERK1/2 and Akt. Importantly, Cmpd17b (but not Cmpd43) favours bias away from intracellular Ca2+ mobilisation in this context, which has been associated with greater cardioprotection in response to Cmpd17b over Cmpd43. However, it is unknown whether these FPR agonists impact vascular physiology and/or elicit vasoprotective effects in the context of diabetes. First, we localized FPR1 and FPR2 receptors predominantly in vascular smooth muscle cells in the aortae of male C57BL/6 mice. We then analysed the vascular effects of Cmpd17b and Cmpd43 on the aorta using wire-myography. Cmpd17b but not Cmpd43 evoked a concentration-dependent relaxation of the mouse aorta. Removal of the endothelium or blockade of endothelium-derived relaxing factors using pharmacological inhibitors had no effect on Cmpd17b-evoked relaxation, demonstrating that its direct vasodilator actions were endothelium-independent. In aortae primed with elevated K+ concentration, increasing concentrations of CaCl2 evoked concentration-dependent contraction that is abolished by Cmpd17b, suggesting the involvement of the inhibition of Ca2+ mobilisation via voltage-gated calcium channels. Treatment with Cmpd17b for eight weeks reversed endothelial dysfunction in STZ-induced diabetic aorta through the upregulation of vasodilator prostanoids. Our data indicate that Cmpd17b is a direct endothelium-independent vasodilator, and a vasoprotective molecule in the context of diabetes.

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Green tea inhibits cycolooxygenase-2 in non-small cell lung cancer cells through the induction of Annexin-1

Cited by 23 publications

References 26 publications

Green Tea Polyphenol Induces Changes in Cancer-Related Factors in an Animal Model of Bladder Cancer

Green Tea Polyphenol Induces Changes in Cancer-Related Factors in an Animal Model of Bladder Cancer

Annexin Proteins: Novel Promising Targets for Anticancer Drug Development

The Novel Small-molecule Annexin-A1 Mimetic, Compound 17b, Elicits Vasoprotective Actions in Streptozotocin-induced Diabetic Mice

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