The Role of Cyclooxygenase-2, Epidermal Growth Factor Receptor and Aromatase in Malignant Mesothelioma

Galati, Rossella

doi:10.5772/50674

Cited by 4 publications

(5 citation statements)

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“…COX-2 is known as prostaglandin-endoperoxide synthase 2 and is a key regulatory enzyme not only responsible for multiple inflammatory mitogenic, and angiogenic activities, but also strongly involved in the development and progression of cancer [ 27 ]. PGE 2 is known to be a potent endogenous molecule, which binds to E-series prostanoid (EP) receptors [ 26 , 27 ]. In other words, PGE 2 functions as a trigger signal to activate the expression of COX-2 in bystander cells [ 16 , 17 ].…”

Section: Resultsmentioning

confidence: 99%

“…It is known that COX-2-derived PGE 2 can initiate a positive feedback loop to activate epidermal growth factor receptor (EFGR), resulting in enhanced expression of COX-2 and increased synthesis of prostaglandins. However, EGFR and its downstream effectors can be activated independently of COX-2/PGE 2 [ 27 ]. The NFκB/COX-2 pathway is also independent of the COX-2/PGE 2 pathway, and can be activated through hypoxia-inducible factor, HIF-1 [ 8 ].…”

Section: Resultsmentioning

confidence: 99%

“…The production of OH radicals and other reactive oxygen species (ROS) by X-ray irradiation was measured by the oxidant-sensing fluorescent probe 2’,7’-dichlorodihydrofluorescein diacetate (DCFH-DA) [ 27 ]. DCFH-DA solutions (100 μM DCFH-DA in PBS, 044–28241, WAKO, Osaka Japan) were prepared under two sets of conditions: null (TU – ), and with an OH radical scavenger, 100 mM thio-urea (TU + ) (33812–92, Nacalai Tesque Inc., Kyoto, Japan).…”

Section: Methodsmentioning

confidence: 99%

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Radiation quality effects alteration in COX-2 pathway to trigger radiation-induced bystander response in A549 lung carcinoma cells

Kobayashi

Konishi

2018

Journal of Radiation Research

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This study aimed to determine whether the radiation-induced bystander effect (RIBE) is affected by radiation quality. To mimic the different radiation qualities of the direct action (D)/indirect action (ID) ratio, A549 cells were exposed to X-rays, with either 100 mM of the radical scavenger, thio-urea (TU+), or null (TU–). Biological responses in irradiated and bystander cells were compared at equal lethal effects of a 6% survival dose, which was estimated from the survival curves to be 8 Gy and 5 Gy for TU+ and TU–, respectively. Cyclooxygenase-2 (COX-2) expression in TU– irradiated cells increased up to 8 h post-irradiation, before decreasing towards 24 h. The concentration of prostaglandin E2 (PGE2), a primary product of COX-2 and known as a secreted inducible factor in RIBE, increased over 3-fold compared with that in the control at 8 h post-irradiation. Conversely, COX-2 expression and PGE2 production of TU+ irradiated cells were drastically suppressed. These results show that the larger D/ID suppressed COX-2 expression and PGE2 production in irradiated cells. However, in contrast to the case in the irradiated cells, COX-2 expression was equally observed in the TU– and TU+ co-cultured bystander cells, which showed the highest expression levels at 24 h post-irradiation. Taken together, these findings demonstrate that radiation quality, such as the D/ID ratio, may be an important factor in the alteration of signalling pathways involved in RIBE.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Radiation quality effects alteration in COX-2 pathway to trigger radiation-induced bystander response in A549 lung carcinoma cells

Kobayashi

Konishi

2018

Journal of Radiation Research

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“…E series prostanoid receptors named EP1, EP2, EP3 and EP4 are repeatedly co‐expressed in the identical cell type and use differently. Stimulation of EP2 and EP4 receptors in Prostaglandin E2 involves the epidermal growth factor receptor (EGFR) for the transactivation to promote tumorigenesis that enhance the cell proliferation, angiogenesis, suppression of immune system, stimulation of cell growth and apoptosis (Galati, 2012).…”

Section: Mechanism Of Cox‐2mentioning

confidence: 99%

Cyclooxygenase‐2 as a therapeutic target against human breast cancer: A comprehensive review

Sahu

Raza

Pradhan

et al. 2023

WIREs Mechanisms of Disease

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Cyclooxygenase-2 (COX-2) is a key aspect of the physiology and pathogenesis of various cancer types. Overexpression of this enzyme is responsible for the elevated prostaglandin production and characteristic feature of breast cancer.Inhibition of COX-2 derived prostanoids facilitates anti-inflammatory, analgesic, and antipyretic effects of non-steroid anti-inflammation drugs. The overexpression of COX-2 is associated with inflammation, pain, and fever. The present study provides the updated relevant literature describing the role of well-characterized isoforms of cyclooxygenase with particular emphasis on COX-2, mechanism of action, the effect of the drug, combinatorial drugs, and microarray-based differential expression analysis and network analysis. We have discussed the currently used combinatorial treatments and their challenges in breast cancer.

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“…HBEGF belongs to the epidermal growth factor family (Prigent and Lemoine, 1992;Raab and Klagsbrun, 1997) and induces downstream transcriptional changes (Korotkevych et al, 2015). By binding to the ErbB3 receptor, HBEGF may indirectly induce proliferation, cell migration, differentiation, or apoptosis (Citri and Yarden, 2006;Galati, 2012). IP astrocytes are thought to require HBEGF to prevent apoptosis (Foo et al, 2011), yet we found that astrocytes proliferate less without HBEGF, but still survive.…”

Section: Astrocyte Morphology and Protein Expression Depend On The Me...mentioning

confidence: 78%

Molecular Mechanisms of Astrocyte Vesicle Fusion at Synaptic Interfaces

Wolfes¹

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Astrocytes are key to neuronal trophic support, development, and synaptic signalling and plasticity. Astrocytes can detect synaptic events at tripartite synapses -a major site of bidirectional communication between neurones and astrocytes-and alter synaptic function by gliotransmitter release. This is reflected in basic research studies as well as ne urodevelopmental disease models, where astrocyte-derived factors shape synapse structure and function. Despite the many roles of astrocytes in brain (patho-) physiology, the mechanisms that underlie release of gliotransmitters to affect astro-neuronal communication are poorly understood.To investigate astrocytic signalling at synaptic interfaces and which molecules mediate astrocytic vesicle fusion, I developed a simple and economical protocol for growing more "in vivo-like" astrocyte monocultures. In comparison to other astrocyte monocultures, spontaneous Ca 2+ signalling in astrocytes of my protocol was more similar to that of astrocytes co-cultured with neurones. Moreover, I observed distinct subcellular domains in which different Ca 2+ event types occurred that were similar to those of astrocytes in slices and in vivo.Using this culture protocol, I confirmed that astrocytes express several vesicleassociated proteins, two of which localised to two distinct vesicle populations that underwent recycling: Vamp2 and Syt7. Vamp2 was previously found in astrocytes, and cleaving Vamp2 by clostridial toxins blocks Ca 2+ -dependent glutamate release from astrocytes. Syt7, which is implicated in lysosomal secretion in different cell types (but also regulates synaptic vesicle replenishment), is a Ca 2+ sensor with high Ca 2+ affinity that has not yet been reported in astrocytes. The Ca 2+ signalling patterns I observed in cultured astrocytes provide a context for Syt7-mediated vesicle fusion, which I further investigated using Syt7 -/mouse cultures: When co-cultured with Syt7 -/astrocytes, wild-type neurones had fewer synapses. Further, I showed that Syt7 and the synaptogenic factor Hevin are developmentally regulated and partially colocalise in cultured astrocytes. These data suggest that Syt7 may regulate vesicular Hevin release from astrocytes, which in turn shapes how neuronal circuits develop. Astrocytic exocytosis contributes to neurodevelopmental diseases, where aberrant astrocytic Hevin release has been implicated in epileptogenesis. Together, these data support that astrocytic Syt7 (and perhaps other Syts) may mediate the release of astrocytic factors that are important for brain development.[K + ] is quickly dispersed through gap junctions to other astrocytes, and finally released into the bloodstream (Walz, 2000). Astrocytes also take up excess glutamate. Like faulty K + buffering, excess extracellular glutamate can also contribute to epilepsy by causing hyperexcitation and seizures, and is cytotoxic at high concentrations (Seifert and Steinhäuser, 2013). Interestingly, clinical hallmarks of epileptic patients also include dysfunctional astrocytic glutamate transpo...

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The Role of Cyclooxygenase-2, Epidermal Growth Factor Receptor and Aromatase in Malignant Mesothelioma

Cited by 4 publications

References 65 publications

Radiation quality effects alteration in COX-2 pathway to trigger radiation-induced bystander response in A549 lung carcinoma cells

Radiation quality effects alteration in COX-2 pathway to trigger radiation-induced bystander response in A549 lung carcinoma cells

Cyclooxygenase‐2 as a therapeutic target against human breast cancer: A comprehensive review

Molecular Mechanisms of Astrocyte Vesicle Fusion at Synaptic Interfaces

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