The functional <i>Aquaporin 1</i>
 −783G/C-polymorphism is associated with survival in patients with glioblastoma multiforme

Hindy, Nicolai El; Rump, Katharina; Lambertz, Nicole; Zhu, Yuan; Frey, Ulrich H.; Bànkfalvi, Àgnes; Siffert, Winfried; Sure, Ulrich; Adamzik, Michael; Sandalcioglu, I. Erol

doi:10.1002/jso.23421

Cited by 16 publications

(14 citation statements)

References 34 publications

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“…A similar pattern might be suggested by data for the voltage gated Ca 2+ channel, inward rectifier K + channels, and Ca 2+ -activated K + channel classes shown. No distinct correlation between survival and transcript level was evident in this analysis for AQP1 and ClC3 channels, both identified previously as targets of interest in pathological mechanisms of glioblastoma progression (McCoy and Sontheimer, 2007;Cuddapah and Sontheimer, 2010;El Hindy et al, 2013). However, this link between expression and survival is based on small biopsies of heterogeneous tumor masses, and does not rule out potential impacts for any of the channels or synaptic proteins that are enriched in GBM.…”

Section: Transcriptomic Analyses Of Ion Channel Genes Selectively Enrcontrasting

confidence: 65%

Molecular Targets for Combined Therapeutic Strategies to Limit Glioblastoma Cell Migration and Invasion

Yool

Ramesh

2020

Front. Pharmacol.

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The highly invasive nature of glioblastoma imposes poor prospects for patient survival. Molecular evidence indicates glioblastoma cells undergo an intriguing expansion of phenotypic properties to include neuron-like signaling using excitable membrane ion channels and synaptic proteins, augmenting survival and motility. Neurotransmitter receptors, membrane signaling, excitatory receptors, and Ca 2+ responses are important candidates for the design of customized treatments for cancers within the heterogeneous central nervous system. Relatively few published studies of glioblastoma multiforme (GBM) have evaluated pharmacological agents targeted to signaling pathways in limiting cancer cell motility. Transcriptomic analyses here identified classes of ion channels, ionotropic receptors, and synaptic proteins that are enriched in human glioblastoma biopsy samples. The pattern of GBM-enriched gene expression points to a major role for glutamate signaling. However, the predominant role of AMPA receptors in fast excitatory signaling throughout the central nervous system raises a challenge on how to target inhibitors selectively to cancer cells while maintaining tolerability. This review critically evaluates a panel of ligand-and voltage-gated ion channels and synaptic proteins upregulated in GBM, and the evidence for their potential roles in the pathological disease progress. Evidence suggests combinations of therapies could be more effective than single agents alone. Natural plant products used in traditional medicines for the treatment of glioblastoma contain flavonoids, terpenoids, polyphenols, epigallocatechin gallate, quinones, and saponins, which might serendipitously include agents that modulate some classes of signaling compounds highlighted in this review. New therapeutic strategies are likely to exploit evidence-based combinations of selected agents, each at a low dose, to create new cancer cell-specific therapeutics. A BFIGURE 1 | Illustration of a sample distribution of published glioblastoma studies suggesting less than 3% combine three themes (inhibitor, proliferation, motility). Venn diagram (A) summarizing the numbers of published articles on glioblastoma, with key words linked to inhibition,

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Section: Transcriptomic Analyses Of Ion Channel Genes Selectively Enrcontrasting

confidence: 65%

Molecular Targets for Combined Therapeutic Strategies to Limit Glioblastoma Cell Migration and Invasion

Yool

Ramesh

2020

Front. Pharmacol.

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“…AQP1 can effectively and rapidly transport water molecules transmembrane. Recent research has pointed out that AQP1 is associated in the development of nervous system disease, especially in tumor pathogenesis (11 , 12) . Upregulation of AQP1 contributes to enhancement of the invasive potential of glioma cells (12 , 13) .…”

Section: Introductionmentioning

confidence: 99%

Glioma-Associated Oncogene Homolog1 (Gli1)-Aquaporin1 pathway promotes glioma cell metastasis

Liao

et al. 2016

BMB Reports

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Glioma-Associated Oncogene Homolog1 (Gli1) is known to be activated in malignant glioma; however, its downstream pathway has not been fully explained. The aim of this study was to explore the role of Gli1-Aquaporin1 (AQP1) signal pathway in glioma cell survival. Our data suggests that both Gli1 and AQP1 are upregulated in glioma tissues, as in comparison to in normal tissues. These up-regulation phenomena were also observed in glioma U251 and U87 cells. It was demonstrated that Gli1 positively regulated the AQP1 expression. By luciferase reporter gene and ChIP assay, we observed that this modulation process was realized by combination of Gli1 with AQP1 promotor. In addition, knock down of Gli1 by siRNA interference reduced the viability of glioma cells as well as suppressed cell metastasis. Also, the inhibitory effects of cell survival by silenced Gli1 were abrogated by AQP1 overexpression. In summary, glioma cell survival is a regulatory process and can be mediated by Gli1-AQP1 pathway. [BMB Reports 2016; 49(7): 394-399]

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“…For example, AQP1 has been revealed to be overexpressed in glioblastoma multiforme, adenoid cystic carcinoma, renal cell carcinoma and breast cancer (32)(33)(34)(35)(36)(37). There have also been previous studies using AQP inhibitor or RNA interference to inhibit AQP1 expression in cancer cells (38).…”

Section: Discussionmentioning

confidence: 99%

Effect of selective inhibition of aquaporin 1 on chemotherapy sensitivity of J82 human bladder cancer cells

Zhang

Chen²,

Dong³

et al. 2018

Oncol Lett

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Abstract. The occurrence of resistance to mitomycin C (MMC) often limits its clinical effectiveness. Combination therapy thus is employed to overcome this treatment resistance. The present study aimed to establish a novel J82 bladder cancer cell line so as to study the effect of inhibition of aquaporin 1 (AQP-1) on chemotherapy sensitivity of J82 bladder cancer cells. A novel J82 bladder cancer cell line whose expression of AQP-1 is inhibited was established through transfection of J82 cells with newly constructed recombinant plasmid. The resulting cell line was designated J82-short hairpin (sh)AQP1 and was subjected to further analyses together with J82 cell line. Reverse transcription-polymerase chain reaction was used to quantify the expression of AQP-1mRNA in the cells; cell viability was analyzed with MTT assay and apoptosis was measured by flow cytometry. The expression of cell proliferation and cell apoptosis-associated proteins, proliferating cell nuclear antigen (PCNA), B cell lymphoma 2 (Bcl-2), Bcl-2 associated X protein (Bax) and caspase-3, were detected by Western blot. A statistically significant decrease in the transcription and expression of AQP1 was observed in the J82-shAQP1 cells as compared with J82 cells. J82-shAQP1 cells treated by MMC, also had a lower cell viability than J82 cells treated by MMC and showed enhanced apoptosis. Western blot analysis revealed J82-shAQP1 cells treated by MMC had less expression of PCNA, lower bcl-2/Bax ratio and more expression of caspase-3 as compared with the J82 cells treated by MMC. Selective inhibition of AQP-1 enhanced MMC chemotherapy sensitivity of J82 bladder cancer cells, suggesting combination of AQP-1 inhibition with MMC treatment as a promising treatment strategy to overcome bladder cancer treatment resistance.

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The functional Aquaporin 1 −783G/C-polymorphism is associated with survival in patients with glioblastoma multiforme

Abstract: Our findings suggest the novel AQP1 polymorphism as a survival prognosticator in patients suffering from GBM that could help to identify a subgroup of patients at high risk for death. Further studies are necessary to reveal the exact molecular mechanisms.

Cited by 16 publications

References 34 publications

Molecular Targets for Combined Therapeutic Strategies to Limit Glioblastoma Cell Migration and Invasion

Molecular Targets for Combined Therapeutic Strategies to Limit Glioblastoma Cell Migration and Invasion

Glioma-Associated Oncogene Homolog1 (Gli1)-Aquaporin1 pathway promotes glioma cell metastasis

Effect of selective inhibition of aquaporin 1 on chemotherapy sensitivity of J82 human bladder cancer cells

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