Cigarette smoke and increased COX-2 and survivin levels in exhaled breath condensate of lung cancer patients: How hot is the link?

Carpagnano, Giovanna Elisiana; Spanevello, Antonio; Palladino, Grazia Pia; Gramiccioni, Claudia; Ruggieri, Cinzia; Carpagnano, Francesco; Barbaro, Maria Pia Foschino

doi:10.1016/j.lungcan.2009.03.033

Cited by 27 publications

(25 citation statements)

References 25 publications

(28 reference statements)

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“…Importantly, COX-2 is primarily responsible for the synthesis of PGE 2 (14). COX-2 elevates inflammation by increasing vasodilation, vascular permeability, and edema in numerous respiratory diseases, such as ALI, chronic obstructive pulmonary disease, pulmonary fibrosis, and lung cancer (15)(16)(17)(18). Some studies suggest that COX-2 and PGE 2 might be associated with SP-related inflammatory responses.…”

mentioning

confidence: 99%

Substance P Upregulates Cyclooxygenase-2 and Prostaglandin E Metabolite by Activating ERK1/2 and NF-κB in a Mouse Model of Burn-Induced Remote Acute Lung Injury

Sio

Ang

et al. 2010

The Journal of Immunology

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Acute lung injury (ALI) is a major cause of mortality in burn patients, even without direct inhalational injury. Identification of early mediators that instigate ALI after burn and of the molecular mechanisms by which they work are of high importance but remain poorly understood. We previously reported that an endogenous neuropeptide, substance P (SP), via binding neurokinin-1 receptor (NK1R), heightens remote ALI early after severe local burn. In this study, we examined the downstream signaling pathway following SP-NK1R coupling that leads to remote ALI after burn. A 30% total body surface area full-thickness burn was induced in male BALB/c wild-type (WT) mice, preprotachykinin-A (PPT-A) gene-deficient mice, which encode for SP, and PPT-A−/− mice challenged with exogenous SP. Local burn injury induced excessive SP-NK1R signaling, which activated ERK1/2 and NF-κB, leading to significant upregulation of cyclooxygenase (COX)-2, PGE metabolite, and remote ALI. Notably, lung COX-2 levels were abrogated in burn-injured WT mice by L703606, PD98059, and Bay 11-7082, which are specific NK1R, MEK-1, and NF-κB antagonists, respectively. Additionally, burn-injured PPT-A−/− mice showed suppressed lung COX-2 levels, whereas PPT-A−/− mice injected with SP showed augmented COX-2 levels postburn, and administration of PD98059 and Bay 11-7082 to burn-injured PPT-A−/− mice injected with SP abolished the COX-2 levels. Furthermore, treatment with parecoxib, a selective COX-2 inhibitor, attenuated proinflammatory cytokines, chemokines, and ALI in burn-injured WT mice and PPT-A−/− mice injected with SP. To our knowledge, we show for the first time that SP-NK1R signaling markedly elevates COX-2 activity via ERK1/2 and NF-κB, leading to remote ALI after burn.

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mentioning

confidence: 99%

Substance P Upregulates Cyclooxygenase-2 and Prostaglandin E Metabolite by Activating ERK1/2 and NF-κB in a Mouse Model of Burn-Induced Remote Acute Lung Injury

Sio

Ang

et al. 2010

The Journal of Immunology

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“…These mutations may be due to genetic or environmental factors (such as diet, pollution and smoking). Despite the lack of survivin expression in lung tissue of animals studied in this research, two studies that showed the survivin expression in healthy smokers were found 14,15 .…”

Section: P53mentioning

confidence: 58%

“…This result becomes very relevant since current researches have focused efforts on survivin positive expression identification as an evolution key point for carcinogenesis, thus its early detection could help to prevent a future irreversible event 14 .…”

Section: P53mentioning

confidence: 99%

Respiratory immunohistochemical study in rats exposed to cigarette smoke and alcohol

et al. 2015

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PURPOSE:To investigate the effects of exposure to cigarette and alcohol on immunohistochemical disorders caused by these attacks to respiratory system of rats. METHODS:Sixty male Wistar rats in four groups: control, cigarette smoke, alcohol and cigarette smoke + alcohol during 260 days.Immunohistochemistry was performed by researching survivin and protein P53 expressions and apoptotic index in parenchymal lung and trachea using TUNEL technique. RESULTS:There was body growth impairment in all experimental groups. Both smoker groups animals had higher trachea survivin expression and bronchial higher apoptotic index. The trachea apoptotic index was also higher in the cigarette smoke group as well as in the alveoli in the cigarette smoke + alcohol group. The three experimental groups showed negative immunoexpression for P53. CONCLUSIONS: this model resulted in immunohistochemical changes caused mainly by exposure to cigarette smoke. There was a synergistic action between alcohol and tobacco in the growth impairment in animals as well as in the cellular apoptotic index. The positive immunoexpression for tracheal survivin in animals from both groups exposed to tobacco smoke and associated with a negative P53 immunoexpression suggests that despite the aggression, carcinogenesis has not happened yet. In addition, the bronchial higher apoptotic index in smokers may be responsible for emphysema.

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“…21 -29 In these studies, COX-2 and survivin protein were found to be up-regulated and positively correlated with advanced tumour stage. 22,25,26 Another report demonstrated a significant correlation between COX-2 and survivin in primary pterygium. 29 It is not known if such a relationship exists between COX-2 and survivin in UCs.…”

Section: Introductionmentioning

confidence: 99%

Cyclooxygenase-2 and Survivin in Superficial Urothelial Carcinoma of the Bladder and Correlation with Intratumoural Microvessel Density

et al. 2010

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Cigarette smoke and increased COX-2 and survivin levels in exhaled breath condensate of lung cancer patients: How hot is the link?

Cited by 27 publications

References 25 publications

Substance P Upregulates Cyclooxygenase-2 and Prostaglandin E Metabolite by Activating ERK1/2 and NF-κB in a Mouse Model of Burn-Induced Remote Acute Lung Injury

Substance P Upregulates Cyclooxygenase-2 and Prostaglandin E Metabolite by Activating ERK1/2 and NF-κB in a Mouse Model of Burn-Induced Remote Acute Lung Injury

Respiratory immunohistochemical study in rats exposed to cigarette smoke and alcohol

Cyclooxygenase-2 and Survivin in Superficial Urothelial Carcinoma of the Bladder and Correlation with Intratumoural Microvessel Density

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