RNA interference-mediated silencing of aquaporin (AQP)-5 hinders angiogenesis of colorectal tumor by suppressing the production of vascular endothelial growth factor

W, Wang; Li, Q; Yang, Tiehong; Li, D; Fan, Desong; Sun, Hongxia; Bai, Guohui

doi:10.4149/neo_2018_161019n487

Cited by 9 publications

(4 citation statements)

References 37 publications

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“…Inhibition of AQP5 significantly decreases the expression of VEGF, which is critical in tumour angiogenesis, suggesting that increased expression of VEGF is positively associated with angiogenesis (21). In a previous study, AQP5 downregulation in colorectal cancer cells resulted in decreased expression of VEGF and a corresponding inhibition of angiogenesis in HUVEC (35). In line with this previous study, the present study found that supernatant collected from H1299 cells following AQP5 knockdown exhibited reduced HUVEC angiogenesis.…”

Section: Discussionsupporting

confidence: 91%

Aquaporin 5 promotes tumor migration and angiogenesis in non‑small cell lung cancer cell line H1299

et al. 2020

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Non-small cell lung cancer (NSCLC) constitutes the majority of all lung-cancer cases. Aquaporin 5 (AQP5) may be involved in NSCLC by promoting lung-cancer initiation and progression. The present study aimed to determine the role of AQP5 in migration and angiogenesis using NSCLC cells and HUVECs. AQPs 1, 3, 4, 5, 8 and 9 were screened in the NSCLC cell line H1299, and the present results showed that AQP5 mRNA was upregulated compared with the other AQP genes. At the protein level, AQP5 was significantly increased in H1299 cells compared with 16HBE cells. AQP5 knockdown in H1299 cells significantly decreased cell migration compared with untransfected cells, as demonstrated by both Transwell and wound closure assays. The present study further investigated H1299 ability to promote HUVEC vascularisation. The supernatants of both transfected and untransfected H1299 cells were used as conditioned medium for HUVECs, and tube formation was measured. The supernatant of AQP5-downregulated cells exhibited significantly low tube formation potential compared with untransfected cells. Similarly, vascular endothelial growth factor was significantly increased in control cells (si-NC) compared with cells transfected with small interfering RNA targeting AQP5. The present study found that AQP5 downregulation significantly decreased the phosphorylation level of epidermal growth factor receptor and the activity of the ERK1/2 pathway. In summary, the present study suggested that AQP5 influenced migration and angiogenesis in NSCLCs in vitro and may potentially exhibit similar in vivo effects.

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Section: Discussionsupporting

confidence: 91%

Aquaporin 5 promotes tumor migration and angiogenesis in non‑small cell lung cancer cell line H1299

et al. 2020

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“…AQP6 reduction by esiRNA treatment was found to suppress MPM cancer proliferation by about 50%. Similar results have been reported on the reduced proliferation of cancer cell lines by silencing the peroxiporins AQP3, AQP5, and AQP8 [ 62 , 63 , 64 ]. Furthermore, the conditions of oxidative stress, similar to those that occur as a result of the treatment with common chemotherapy treatments, were able to further reduce proliferation, especially in mesothelioma cells.…”

Section: Discussionsupporting

confidence: 88%

Aquaporin-6 May Increase the Resistance to Oxidative Stress of Malignant Pleural Mesothelioma Cells

Pellavio

Martinotti

Patrone

et al. 2022

Cells

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Malignant pleural mesothelioma (MPM) is an aggressive cancer of the pleural surface and is associated with previous asbestos exposure. The chemotherapy drug is one of the main treatments, but the median survival ranges from 8 to 14 months from diagnosis. The redox homeostasis of tumor cells should be carefully considered since elevated levels of ROS favor cancer cell progression (proliferation and migration), while a further elevation leads to ferroptosis. This study aims to analyze the functioning/role of aquaporins (AQPs) as a hydrogen peroxide (H2O2) channel in epithelial and biphasic MPM cell lines, as well as their possible involvement in chemotherapy drug resistance. Results show that AQP-3, -5, -6, -9, and -11 were expressed at mRNA and protein levels. AQP-6 was localized in the plasma membrane and intracellular structures. Compared to normal mesothelial cells, the water permeability of mesothelioma cells is not reduced by exogenous oxidative stress, but it is considerably increased by heat stress, making these cells resistant to ferroptosis. Functional experiments performed in mesothelioma cells silenced for aquaporin-6 revealed that it is responsible, at least in part, for the increase in H2O2 efflux caused by heat stress. Moreover, mesothelioma cells knocked down for AQP-6 showed a reduced proliferation compared to mock cells. Current findings suggest the major role of AQP-6 in providing mesothelioma cells with the ability to resist oxidative stress that underlies their resistance to chemotherapy drugs.

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“…A similar report revealed that downregulation of AQP5 inhibited hepatocellular carcinoma cell invasion and EMT process through modulating EMT-related molecules, such as E-cadherin and N-cadherin (34). Wang et al (35) reported that AQP5 silencing inhibited proliferation, migration and the enzyme activity of MMP-9 in human umbilical vein endothelial cells, but did not affect the enzyme activity of MMP-2. The discrepancy between this previous report and the current study with regards to MMP-2 may have resulted from different detection indexes (i.e.…”

Section: Discussionmentioning

confidence: 85%

Differential expression and inhibitory effects of aquaporins on the development of adenomyosis

et al. 2020

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aquaporin 2 (aQP2), aQP5 and aQP8 participate in adenomyosis (AM). Ηowever, the roles of these three molecules in AM have not been fully elucidated. In the present study, Institute of Cancer Research female mice were used to establish a model of AM. Subsequently, the endometrial tissues of the mice were observed by hematoxylin-eosin staining, and AM severity, uterus diameter, uterus index, ovary index and numbers of nodules on the uterine surface were evaluated and counted. In addition, eutopic and ectopic endometrial stromal cells (ESCs) were isolated from eutopic and ectopic endometrial samples derived from patients with AM and were then identified by immunofluorescence. The viability, and migratory and invasive ability of ESCs transfected with small interfering RNA targeting AQP5 (siAQP5) were determined by Cell Counting Κit-8, scratch wound-healing and Transwell assays, respectively. Reverse transcription-quantitative polymerase chain reaction was performed to determine the mRNA expression levels of AQP5, epithelial-mesenchymal transition (EMT)-related genes (E-and N-cadherin), matrix metalloproteinase (MMP)-2 and-9. Protein expression levels of AQP2, AQP5, AQP8, E-, N-cadherin, MMP-2 and-9 were detected by western blotting. AM severity and uterus index were higher, and there were a greater number of nodules on the uterine surface in the AM group compared with the sham group. AQP2, AQP5 and AQP8 proteins were highly expressed in eutopic and ectopic endometrium of the AM group, and AQP5 was more highly expressed than AQP2 or AQP8. In addition, the data showed that Vimentin was positively expressed in ESCs, and that siAQP5 suppressed the mRNA expression levels of AQP5, cell viability, migration, invasion, EMT and MMP-2 and-9 expression in ESCs. In conclusion, AQP2, AQP5 and AQP8 were highly expressed in eutopic and ectopic endometrium. Notably, AQP5 silencing may suppress AM by inhibiting viability, migration, invasion, EMT, and MMP-2 and-9 expression in ESCs.

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RNA interference-mediated silencing of aquaporin (AQP)-5 hinders angiogenesis of colorectal tumor by suppressing the production of vascular endothelial growth factor

Cited by 9 publications

References 37 publications

Aquaporin 5 promotes tumor migration and angiogenesis in non‑small cell lung cancer cell line H1299

Aquaporin 5 promotes tumor migration and angiogenesis in non‑small cell lung cancer cell line H1299

Aquaporin-6 May Increase the Resistance to Oxidative Stress of Malignant Pleural Mesothelioma Cells

Differential expression and inhibitory effects of aquaporins on the development of adenomyosis

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