Expression of aquaporin 5 in primary carcinoma and lymph node metastatic carcinoma of non-small cell lung cancer

Song, Tingting; Yang, Hong; Ho, James Chung Man; Tang, Sydney C.W.; Sze, Stephen Cho Wing; Lao, Lixing; Wang, Ying; Zhang, Kalin Yanbo

doi:10.3892/ol.2015.3108

Cited by 24 publications

(17 citation statements)

References 22 publications

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“…AQP5 have been found expressed highly in primary human glioma cells compared with normal tissue, this is in accordance with the study that reported AQPs (such as AQP1 , AQP5 and AQP8 ) have been observed in high-grade tumors of various tissues [29, 30]. It is confirmed that high expression of AQP5 was associated with tumor growth, invasion and metastasis in non-small cell lung cancer [31]. Yang et al found that AQP5 expression was increased in borderline ovarian tumors and malignant tumors compared to benign and normal ovarian tumors, and that AQP5 expression was correlated with lymph node metastasis [32].…”

Section: Discussionsupporting

confidence: 89%

Effects of AQP5 gene silencing on proliferation, migration and apoptosis of human glioma cells through regulating EGFR/ERK/ p38 MAPK signaling pathway

et al. 2017

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We investigated the effects of aquaporin 5 (AQP5) gene silencing on the proliferation, migration and apoptosis of human glioma cells through regulating the EGFR/ERK/p38MAPK signaling pathway. qRT-PCR was applied to examine the mRNA expressions of AQP5 in five human glioma cell lines. U87-MG, U251 and LN229 cells were selected and assigned into blank, vector, AQP5 siRNA and FlagAQP5 groups. MTT assay was used to measure cell proliferation. Flow cytometry (FCM) with AnnexinV-FITC/PI double staining and PI staining were employed to analyze cell apoptosis and cell cycle respectively. Scratch test was used to detect cell migration. Western blotting was performed to determine the EGFR/ERK/p38 MAPK signaling pathway-related proteins. Results showed that the positive expression of AQP5 in primary glioblastoma was associated with the tumor size and whether complete excision was performed. The mRNA expressions of AQP5 in cell lines of U87-MG, U251 and LN229 were significantly higher than in U373 and T98G. The proliferation rates of U87-MG, U251 and LN229 cells in the AQP5 siRNA group were lower than in the vector and blank groups. The apoptosis rate increased in the AQP5 siRNA group compared with the vector group. Scratch test demonstrated that AQP5 gene silencing could suppress cell migration. Compared with the vector and blank groups, the AQP5 siRNA group showed decreased expressions of the ERK1/2, p38 MAPK, p-ERK1/2 and p-p38 MAPK proteins. AQP5 gene silencing could inhibit the cell proliferation, reduce cell migration and promote the cell apoptosis of U87-MG, U251 and LN229 by suppressing EGFR/ERK/p38 MAPK signaling pathway.

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Section: Discussionsupporting

confidence: 89%

Effects of AQP5 gene silencing on proliferation, migration and apoptosis of human glioma cells through regulating EGFR/ERK/ p38 MAPK signaling pathway

et al. 2017

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“…Based on the findings of relationships between heat shock, cell volume, apoptosis, and proliferation, molecules related to cell volume regulation, e.g., potassium, chloride channels, the potassium and chloride co-transporter (KCC), and AQPs, may play an important role in the anticancer effects of HT. These molecules, e.g., KCC3, and AQP5, were found to be overexpressed in human cancer samples, and were identified as prognostic factors (11)(12)(13)(14)(15)32,33). If HT regulates these molecules, targeted therapy to tumors overexpressing these molecules may become possible.…”

Section: Discussionmentioning

confidence: 99%

“…The expression of AQPs has been detected in several types of tumors, and AQPs are receiving increasing attention as new biomarkers or therapeutic targets (9,10). Previous studies reported that the expression of AQP5 was altered in tumors of various organs such as the esophagus, lung, prostate, liver, stomach, breast, and gallbladder (11)(12)(13)(14)(15)(16)(17). The strong expression of AQP5 has been identified as a prognostic factor in human cancer samples (11)(12)(13)(14)(15).…”

Section: Introductionmentioning

confidence: 99%

“…Previous studies reported that the expression of AQP5 was altered in tumors of various organs such as the esophagus, lung, prostate, liver, stomach, breast, and gallbladder (11)(12)(13)(14)(15)(16)(17). The strong expression of AQP5 has been identified as a prognostic factor in human cancer samples (11)(12)(13)(14)(15). In an in vitro study, the downregulated expression of AQP5 was shown to suppress cancer cell proliferation and survival via the regulation of p21 (11), while the upregulated expression of AQP5 promoted cancer proliferation (15).…”

Section: Introductionmentioning

confidence: 99%

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Heat shock exerts anticancer effects on liver cancer via autophagic degradation of aquaporin 5

Kudou

Shiozaki

Kosuga

et al. 2017

International Journal of Oncology

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Previous studies described that the expression of aquaporin 5 (AQP5) was altered in tumors of various organs. AQP5 is attracting attention as a new cancer therapeutic target. In the present study, heat shock-induced changes in AQP5 expression were evaluated by immunofluorescent staining (IF) and western blotting (WB) of liver cancer cells. AQP5 knockdown experiments or a heat shock treatment were conducted, and their effects on cell volume, proliferation, cell cycle, the activity of apoptosis and migration/invasion were compared. Cycloheximide (CHX) chase experiments and double IF of AQP5 and light chain 3B (LC3B) were performed to investigate the mechanisms underlying changes in AQP5 expression. The results showed that IF and WB revealed decrease in AQP5 expression on cellular membranes and in the cytoplasm of heated cells. AQP5 knockdown and heat shock similarly decreased cell volume, suppressed migration/invasion and proliferation, and induced early apoptosis and partial G0/G1 arrest. CHX chase experiments revealed that heat shock accelerated the degradation of AQP5, which was rescued under CHX and the autophagy inhibitor, bafilomycin A1 (BafA1). Double IF showed the co-localization of AQP5 and LC3B on BafA1-treated heated cells. In conclusion, we demonstrated that heat shock decreased AQP5 on cellular membranes and in the cytoplasm by activating autophagic degradation, and heat shock and AQP5 knockdown exerted similar anticancer effects, suggesting that heat shock exerts anticancer effects via the autophagic degradation of AQP5.

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“…AQP5 is expressed in multiple secretory organs, including salivary glands, pancreas, and sweat glands (6,30,35). AQP5 is ectopically expressed or overexpressed in several cancers including breast (12,13) and lung cancer (7,40,51), where expression levels correlate with poor prognosis (7,13). Moreover, in prostate cancer (19,34), non-small cell lung cancer (40), colon cancer (14), and cervical cancer (49), overexpression of AQP5 correlates with metastases to lymph nodes.…”

Section: Introductionmentioning

confidence: 99%

Ectopic expression of aquaporin-5 in noncancerous epithelial MDCK cells changes cellular morphology and actin fiber formation without inducing epithelial-to-mesenchymal transition

Jensen

Holst

et al. 2018

American Journal of Physiology-Cell Physiology

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Aquaporin-5 (AQP5) is a plasma membrane water channel mainly expressed in secretory glands. Increased expression of AQP5 is observed in multiple cancers, including breast cancer, where high expression correlates with the degree of metastasis and poor prognosis. Moreover, studies in cancer cells have suggested that AQP5 activates Ras signaling, drives morphological changes, and in particular increased invasiveness. To design intervention strategies, it is of utmost importance to characterize and dissect the cell biological changes induced by altered AQP5 expression. To isolate the effect of AQP5 overexpression from the cancer background, AQP5 was overexpressed in normal epithelial MDCK cells which have no endogenous AQP5 expression. AQP5 overexpression promoted actin stress fiber formation and lamellipodia dynamics. Moreover, AQP5 decreased cell circularity. Phosphorylation of AQP5 on serine 156 in the second intracellular loop has been shown to activate the Ras pathway. When serine 156 was mutated to alanine to mimic the nonphosphorylated state, the decrease in cell circularity was reversed, indicating that the AQP5-Ras axis is involved in the effect on cell shape. Interestingly, the cellular changes mediated by AQP5 were not associated with induction of epithelial-to-mesenchymal transition. Thus, AQP5 may contribute to cancer by altering cellular morphology and actin organization, which increase the metastatic potential.

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Expression of aquaporin 5 in primary carcinoma and lymph node metastatic carcinoma of non-small cell lung cancer

Cited by 24 publications

References 22 publications

Effects of AQP5 gene silencing on proliferation, migration and apoptosis of human glioma cells through regulating EGFR/ERK/ p38 MAPK signaling pathway

Effects of AQP5 gene silencing on proliferation, migration and apoptosis of human glioma cells through regulating EGFR/ERK/ p38 MAPK signaling pathway

Heat shock exerts anticancer effects on liver cancer via autophagic degradation of aquaporin 5

Ectopic expression of aquaporin-5 in noncancerous epithelial MDCK cells changes cellular morphology and actin fiber formation without inducing epithelial-to-mesenchymal transition

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