Overexpression of AQP1 in Lung Adenocarcinomas and Pleural Mesoendotheliomas.

López-Campos, JL; Silva, R Sanchez; Izquierdo, Lourdes Gómez; Cejudo, P; Martin, Evangeline M.; Ortega, Francisco G.; Aral, J Toledo; Barrot, Emilia; Echevarría, Miriam

doi:10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2682

Cited by 13 publications

(16 citation statements)

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“…The first member aquaporin-1 (AQP1) is present throughout many cell types such as epithelial, endothelial, microvascular endothelial beds outside of the brain, as well as a variety of tumor cells [3]. Recently, intensive studies have been focused on the modulation of AQP1 expression in tumor cells and its effects on tumorigenesis, tumor growth and progression 270 [4,5]. According to clinical analysis, AQP1 expression might be regarded as a new molecular prognostic marker in patients with renal cell carcinoma [6].…”

Section: Introductionmentioning

confidence: 99%

Hypoxia-induced Up-regulation of Aquaporin-1 Protein in Prostate Cancer Cells in a p38-dependent Manner

Tie

Lü

Pan

et al. 2012

Cell Physiol Biochem

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Background/Aims: Aquaporin-1 (AQP1) is a glycoprotein that mediates osmotic water transport, its expression has been found to correlate with tumour stage in some tumours. However, the mechanism by which AQP1 protein expression is regulated in tumor cells remains to be fully elucidated. We hypothesized that hypoxia might play an important role in AQP1 induction during tumorigenesis and at the late stages of tumor development. Methods: Isotonic and serum-free hypoxic models were used to investigate AQP1 expression in PC-3M human prostate cancer cells. Results: AQP1 expression was up-regulated by density-induced pericellular hypoxia and cobalt(II) chloride (CoCl₂)-induced hypoxia at the transcriptional level. Moreover, phosphorylation of p38 mitogen-activated protein kinase (MAPK) was induced by density-induced pericellular hypoxia and CoCl₂-induced hypoxia, specific inhibitors of p38 MAPK could concentration-dependently block those effects of hypoxia on AQP1 expression. Intracellular calcium ion (Ca²⁺) and protein kinase C (PKC) were shown to be responsible for the activation of p38 MAPK pathway. In addition, AQP1 induction in dense cultures was dependent on lowered oxygen (O₂) tension. In high cell density culture, certain secretory proteins might induce AQP1 expression indirectly. Conclusion: These findings suggest that AQP1 could be induced by hypoxia at transcription level, and the regulation of AQP1 in PC-3M cells is dependent on calcium, PKC and p38 MAPK, as well as low oxygen tension.

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Section: Introductionmentioning

confidence: 99%

Hypoxia-induced Up-regulation of Aquaporin-1 Protein in Prostate Cancer Cells in a p38-dependent Manner

Tie

Lü

Pan

et al. 2012

Cell Physiol Biochem

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“…It provides a functional explanation for AQP expression in tumor cells and for the correlations between tumor shift and AQP expression. Additionally, it provides a rational basis to evaluate AQP inhibitors, when available, for tumor therapy, both for reduction of tumor development and tumor spread (30).…”

Section: Discussionmentioning

confidence: 99%

Reduced migration of Ishikawa cells associated with downregulation of aquaporin-5

Jiang

Yan

et al. 2012

Oncology Letters

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Abstract. Aquaporin (AQP)-dependent cell migration has broad implications in angiogenesis, tumor metastasis, wound healing, glial scarring and other events requiring cell movement. There are 13 isoforms of AQP (0-12) that have been identified in mammals. It is unclear whether AQP5 plays a role in the development of endometrial cancer. We recently demonstrated that ovarian steroids may affect the expression of AQP5 in the female genital tract. In this study, we considered whether AQP5 may affect cell migration in Ishikawa cells, an adenocarcinoma cell line derived from the endometrium. The results showed that the downregulation of AQP5 results in reduced Ishikawa cell migration. The estrogen (E2) receptor in the promoter of AQP5 mediated the regulation of AQP5 expression in the normal endometrium and endometrial cancer. By contrast, the upregulation of AQP5 by E2 increased cell migration, invasion and adhesion through increased annexin-2, which is responsible for F-actin remodeling and rearrangement. E2 regulates Ishikawa cell migration by regulating the AQP5 expression.

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“…The evidence that AQP1 was overexpressed in pleural mesothelioma was provided by López-Campos et al [60], who claimed AQP1 overexpression that probably occurred in a HIF-dependent manner might confer to tumor cells a competitive phenotype, which could lead to its unfavorable influence on the development of MPM. Recently, two independent MPM cohorts consisting of 80 patients who underwent extrapleural pneumonectomy (EPP) and 56 patients who were treated conservatively were studied to investigate the relationship between AQP1 expression by immunohistochemistry (IHC) and OS [61].…”

Section: Aquaporin 1 (Aqp1)mentioning

confidence: 99%

“…In this research study, expression of AQP1 by >50 % of tumor cells was associated with significantly enhanced survival in both cohorts in univariate and multivariate analysis, presenting AQP1 as an independent favorable prognostic predictor, regardless of the type of treatment received or established prognostic factors. However, this finding appeared to be paradoxical, because upregulation of the AQP1 that is shown to increase the aggressiveness of malignant cells [60] has an unexpected beneficial impact on the survival of MPM patients. Accordingly, Jagirdar et al [55] came up with a hypothesis that AQP1 might upregulate the clearance of excess pleural fluid from the pleural cavity leaving less space for the malignant mesothelial cells to migrate and invade new foci in the cavity, therefore impeding the propagation of the tumor in the pleura.…”

Section: Aquaporin 1 (Aqp1)mentioning

confidence: 99%

Prognostic value of several biomarkers for the patients with malignant pleural mesothelioma

Liu

Jiao

et al. 2015

Tumor Biol.

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Malignant pleural mesothelioma (MPM) is a highly aggressive tumor of the pleura closely related to asbestos exposure. Rare as it is, the incidence of MPM is predicted to increase mainly as a result of a lengthy latency period from the initial asbestos exposure, making it a public health concern for the next decades. Moreover, the patients with MPM have an extremely poor prognosis due to its high resistance to conventional oncologic treatments and delayed diagnosis. Although the result of current therapeutic modalities based on patient features and clinical stages is very frustrating, great advances have been shown in the knowledge of molecular biology of MPM in recent years. This is accompanied by dozens of putative prognostic biomarkers that are actively involved in tumor biological activities. These prognostic candidates can offer us a new insight into the biological characteristics of MPM, contributing to development of individualized therapeutic strategies directed against oncogenesis and tumor progression. Thus, personalized approaches based on the molecular biology of the patient's tissue or body fluid will potentially improve the present disappointing outcome, bringing new hope for patients with MPM. This article reviews the principal and several novel biomarkers that can have an influence on prognosis, in the hope that they can provide us with a more profound understanding of the biology of this lethal disease.

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Overexpression of AQP1 in Lung Adenocarcinomas and Pleural Mesoendotheliomas.

Cited by 13 publications

References 0 publications

Hypoxia-induced Up-regulation of Aquaporin-1 Protein in Prostate Cancer Cells in a p38-dependent Manner

Hypoxia-induced Up-regulation of Aquaporin-1 Protein in Prostate Cancer Cells in a p38-dependent Manner

Reduced migration of Ishikawa cells associated with downregulation of aquaporin-5

Prognostic value of several biomarkers for the patients with malignant pleural mesothelioma

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