Upregulation of heme oxygenase-1 in oral epithelial dysplasias

Lee, J.; Lee, S.-K.; Lee, B.-U.; Lee, H.-J.; Cho, N.-P.; Yoon, Ju Hwa; Choi, H.-R.; Kim, E.-C.

doi:10.1016/j.ijom.2007.07.028

Cited by 24 publications

(25 citation statements)

References 26 publications

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“…It would be interesting to know if the presence of COPD influences the HO-1 levels in non-malignant areas adjacent to the tumors. Additionally, we observed that preneoplastic tissues showed similar levels of HO-1 than tumor epithelia, supporting the results obtained in oral epithelial dysplasias [38].…”

Section: Discussionsupporting

confidence: 90%

“…These results are in accordance with those obtained for other tissues, in which upregulation of HO-1 in tumors was observed when compared with normal tissues [9,21]. For example, in prostate cancer [22,23], brain tumors [24], chronic myeloid leukemia [25], melanoma [26], pancreatic cancer [27], renal carcinoma [28] and head and neck squamous cell carcinoma [29,30] HO-1 has been shown to be overexpressed. Our results do support those of De Palma et al [20] showing down regulation of HO-1 in NSCLC tumors at the mRNA level.…”

Section: Discussionsupporting

confidence: 89%

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Expression of heme oxygenase-1 in non-small cell lung cancer (NSCLC) and its correlation with clinical data

et al. 2012

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While changes in heme oxygenase (HO-1) in lung cancer have already been reported, conflicting results were obtained for enzyme expression in human lung cancer specimens. Therefore, the aim of this work was to study HO-1 expression in a large collection of human lung cancer samples. For this purpose, we analyzed the expression of HO-1 in an organized tissue microarray (TMA) and investigated its correlation with clinicopathological data. Ninety-six percent of tumor samples were positive for HO-1, and the expression of HO-1 was significantly higher in cancerous than in non-cancerous tissues. Importantly, HO-1 expression correlated with advanced stages and lymph node involvement. Additionally, quantitative RT-PCR in 18 pairs of human lung carcinomas and their adjacent non-malignant tissues was performed. Our results demonstrate that HO-1 protein is upregulated in epithelial malignant cells in NSCLC and its expression is associated with higher stages of the disease. Additionally, different subcellular localization is observed between tumor and adjacent non-malignant tissues.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionsupporting

confidence: 89%

Expression of heme oxygenase-1 in non-small cell lung cancer (NSCLC) and its correlation with clinical data

et al. 2012

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“…Treatment such as chemotherapy, radiation, or photodynamic therapy may increase HMOX1 level in cancer cells (18,40). Moreover, in comparison to the surrounding healthy tissues, HMOX1 expression is increased in different types of tumors, such as melanoma (47), glioblastoma (6), Kaposi sarcoma (36), or squamous cell carcinoma (SCC) (25,49). Conversely, diminished HMOX1 expression was shown in human early-stage tumor specimens of non-small cell lung carcinoma (NSCLC) (5), suggesting an opposite HMOX1 role in different neoplasms.…”

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confidence: 99%

Interplay Between Heme Oxygenase-1 and miR-378 Affects Non-Small Cell Lung Carcinoma Growth, Vascularization, and Metastasis

Skrzypek

Tertil

Gołda

et al. 2013

Antioxidants & Redox Signaling

134

139

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Aims: Heme oxygenase-1 (HO-1, HMOX1) can prevent tumor initiation; while in various tumors, it has been demonstrated to promote growth, angiogenesis, and metastasis. Here, we investigated whether HMOX1 can modulate microRNAs (miRNAs) and regulate human non-small cell lung carcinoma (NSCLC) development. Results: Stable HMOX1 overexpression in NSCLC NCI-H292 cells up-regulated tumor-suppressive miRNAs, whereas it significantly diminished the expression of oncomirs and angiomirs. The most potently down-regulated was miR-378. HMOX1 also up-regulated p53, down-regulated angiopoietin-1 (Ang-1) and mucin-5AC ( MUC5AC), reduced proliferation, migration, and diminished angiogenic potential. Carbon monoxide was a mediator of HMOX1 effects on proliferation, migration, and miR-378 expression. In contrast, stable miR-378 overexpression decreased HMOX1 and p53; while enhanced expression of MUC5AC, vascular endothelial growth factor (VEGF), interleukin-8 (IL-8), and Ang-1, and consequently increased proliferation, migration, and stimulation of endothelial cells. Adenoviral delivery of HMOX1 reversed miR-378 effect on the proliferation and migration of cancer cells. In vivo, HMOX1 overexpressing tumors were smaller, less vascularized and oxygenated, and less metastatic. Overexpression of miR-378 exerted opposite effects. Accordingly, in patients with NSCLC, HMOX1 expression was lower in metastases to lymph nodes than in primary tumors. Innovation and Conclusion: In vitro and in vivo data indicate that the interplay between HMOX1 and miR-378 significantly modulates NSCLC progression and angiogenesis, suggesting miR-378 as a new therapeutic target. Rebound Track: This work was rejected during standard peer review and rescued by Rebound Peer Review (Antioxid Redox Signal 16, 293-296, 2012) with the following serving as open reviewers:

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“…However, they might be produced in excess in chronic inflammatory processes and, thus, exert detrimental effects, such as lipid peroxidation and DNA damage. The progression of oxidative stress damage has been implicated in human cancer 27,32 . In distal esophagus, Sihvo et al 15 observed that the reflux diseasemetaplasia-carcinoma sequence revealed progressively increased oxidative stress, which suggested a link between oxidative damage and malignant transformation of esophageal epithelium.…”

Section: Discussionmentioning

confidence: 99%

“…Therefore, malignant behavior and HO-1 expression may be associated, and an elevated HO-1 activity has been found in cells of renal adenocarcinoma, lymphosarcoma, hepatoma, melanoma and squamous carcinoma [23][24][25][26] . A recent study demonstrated that HO-1 expression is progressively elevated following the sequence from normal oral epithelium to epithelia dysplasia and, finally, to squamous cell cancer in humans 27 . These findings reinforce the idea that oxidative stress may also play an important role in esophageal squamous cell carcinogenesis.…”

Section: Introductionmentioning

confidence: 99%

Evaluation of the heme oxygenase-1 expression in esophagitis and esophageal cancer induced by different reflux experimental models and diethylnitrosamine

et al. 2010

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Purpose:To study the expression of heme-oxygenase-1 (HO-1), an enzyme induced by oxidative stress, in specimens obtained from an experimental model in rats that evaluated the role of gastric and duodenal reflux in esophageal carcinogenesis. Methods: Esophageal specimens embedded in paraffin obtained from different experimental groups of rats were used for immunohistochemistry analysis of HO-1 expression. The rats had been divided into the following groups and were killed after 22 weeks: (1) cardioplasty to induce acid reflux; (2) esophagoduodenal anastomosis to induce duodenal reflux; (3) no treatment; (4) cardioplasty + diethylnitrosamine (DEN); (5) esophagoduodenal anastomosis + DEN; and (6) DEN. The study sample comprised 3 specimens from each group with the most severe histopathological lesions found on each study branch. Results: The expression of HO-1 was seen only in rat specimens submitted to esophagoduodenal anastomosis (Groups 2 and 5), and the analysis of mean fluorescence intensity revealed a significant increase of HO-1 expression (4.8 and 4.6 fold, respectively) when compared with the control group (Group 3) (p<0.05). The main target for HO-1 induction was the inflammatory cells inside the tumor or in subepithelial areas. Rats exposed to gastric reflux had no HO-1 expression. Conclusions: Reflux esophagitis induced by reflux of duodenal contents, which provoked considerable oxidative stress, may play an important role in esophageal carcinogenesis. Acid reflux did not induce oxidative stress in this experimental model. Key words: Heme Oxygenase-1. Oxidative Stress. Esophageal Neoplasms. Rats. RESUMOObjetivo: Estudar a expressão da HO-1 (enzima induzida pelo estresse) em diferentes peças esofágicas obtidas de um estudo experimental em ratos que avaliou o papel do refluxo gastroesofágico e duodeno esofágico na carcinogênese experimental. Métodos: Blocos de parafina contendo peças de esôfago provenientes de um estudo experimental com ratos foram utilizados para verificar a expressão imunohistoquímica da HO-1. Os ratos haviam sido divididos nos seguintes grupos: (1) Cardioplastia com o objetivo de promover refluxo ácido, (2) Anastomose esofagoduodenal para indução de refluxo misto (ácido e biliar), (3) sem tratamento (controles), (4) cardioplastia + dietil-nitrosamina (DEN), (5) Anastomose esofagoduodenal + DEN, (6) DEN. Amostras contendo três peças de cada grupo com as lesões histopatológicas mais graves encontradas em cada braço do estudo foram escolhidas para avaliação da expressão imunoistoquímica da HO-1. Resultados: A expressão da HO-1 foi observada somente nas peças de esôfago de ratos submetidos à anastomose esofagoduodenal (Grupos 2 e 5) e analise da intensidade média da fluorescência demonstrou uma diferença significativa na expressão da HO-1 nesses grupos quando comparada com o grupo controle (4,8 e 4,6 vezes respectivamente) (p<0,05). As células inflamatórias localizadas dentro dos tumores e nas regiões adjacentes ao epitélio foram as que mais intensamente expressaram a HO-1. Ratos ...

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Upregulation of heme oxygenase-1 in oral epithelial dysplasias

Cited by 24 publications

References 26 publications

Expression of heme oxygenase-1 in non-small cell lung cancer (NSCLC) and its correlation with clinical data

Expression of heme oxygenase-1 in non-small cell lung cancer (NSCLC) and its correlation with clinical data

Interplay Between Heme Oxygenase-1 and miR-378 Affects Non-Small Cell Lung Carcinoma Growth, Vascularization, and Metastasis

Evaluation of the heme oxygenase-1 expression in esophagitis and esophageal cancer induced by different reflux experimental models and diethylnitrosamine

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