Effect of AQP9 Expression in Androgen-Independent Prostate Cancer Cell PC3

Chen, Qiwei; Zhu, Liang; Zheng, Bo; Wang, Jinliang; Song, Xishuang; Zheng, Wei; Wang, Lina; Yang, Deyong; Wang, Jianbo

doi:10.3390/ijms17050738

Cited by 20 publications

(20 citation statements)

References 23 publications

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“…However, the mRNA expression of AQP9 is upregulated in breast cancer, and high AQP9 expression may be related to worse relapse-free survival in that disease ( Zhu et al, 2019 ). Chen et al (2016) have demonstrated that the expression of AQP9 is detectable in prostate cancer cells, whereas inhibition of its expression impedes their growth and promotes cell apoptosis through effects on the extracellular regulated protein kinase signaling pathway. AQP9 also functions as an oncogene in astrocytoma by facilitating cell invasion and motility via the AKT pathway ( Lv et al, 2018 ).…”

Section: Discussionmentioning

confidence: 99%

RETRACTED: Long Non-coding RNA LINC00320 Inhibits Tumorigenicity of Glioma Cells and Angiogenesis Through Downregulation of NFKB1-Mediated AQP9

Chang

Bian

Xiong

et al. 2020

Front. Cell. Neurosci.

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The inhibitory effect of long intergenic non-coding RNA 00320 (LINC00320) in glioma cell proliferation has been proposed in a recent study. However, the mechanisms by which LINC00320 regulate aquaporin 9 (AQP9) in glioma require further exploration. Hence, this study aims to investigate effects of LINC00320 on tumorigenicity of glioma cells and angiogenesis of microvascular endothelial cells (MVECs). Expression of LINC00320 and AQP9 in glioma tissues and cells was measured by reverse transcription–quantitative polymerase chain reaction and Western blot analysis. The relationship among LINC00320, nuclear factor κB subunit 1 (NFKB1) and AQP9 was examined by RNA immunoprecipitation, dual-luciferase reporter gene, and chromatin immunoprecipitation assays. The participation of LINC00320 and AQP9 in glioma cell proliferation and MVEC angiogenesis was analyzed using gain- and loss-of-function approaches. Finally, a nude mouse orthotopic xenograft model of glioma was established to investigate the effects of LINC00320 and AQP9 on glioma growth in vivo. LINC00320 was under-expressed and AQP9 was over-expressed in glioma tissues. Further mechanistic investigation showed that LINC00320 downregulated AQP9 by inhibiting the recruitment of NFKB1 to the promoter region of AQP9. LINC00320 overexpression or AQP9 silencing inhibited the proliferation of glioma cells and angiogenesis of MVECs. Also, upregulation of LINC00320 restrained tumor growth and angiogenesis in xenograft mice by downregulating AQP9. Taken together, LINC00320 acts as a tumor suppressor in glioma, thus presenting a novel therapeutic target.

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Section: Discussionmentioning

confidence: 99%

RETRACTED: Long Non-coding RNA LINC00320 Inhibits Tumorigenicity of Glioma Cells and Angiogenesis Through Downregulation of NFKB1-Mediated AQP9

Chang

Bian

Xiong

et al. 2020

Front. Cell. Neurosci.

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“…Increases or decreases in AQP9 expression have been detected in different tumor types. AQP9 is significantly enhanced in prostate cancer tissues than that in adjacent cancer tissues (14); however, AQP9 levels are reduced in human hepatocellular carcinoma compared with the paratumoral normal liver tissues (15). The present study demonstrated that AQP9 was expressed in astrocytoma cells, indicating that AQP9 may be involved in astrocytoma cell progression.…”

Section: Discussionmentioning

confidence: 47%

“…It is reported that AQP9 contributes to cell growth and invasion of prostate cancer cells (14). However, AQP9 can suppress hepatoma cell invasion in vitro and xenograft tumor growth in vivo (16).…”

Section: Discussionmentioning

confidence: 99%

AQP9 promotes astrocytoma cell invasion and motility via the AKT pathway

Huang

Dai

et al. 2018

Oncol Lett

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Abstract. The aquaporin (AQP) family, which includes 13 members identified in mammalian cells, is involved in cancer development and progression. AQP9 expression is upregulated in several tumor tissue types. However, the functions of AQP9 in astrocytoma remain elusive. The present study identified that AQP9 was expressed in astrocytoma cells. AQP9 expression was silenced by transfection with small interfering RNAs and increased by transfection with a plasmid containing the AQP9 gene. Using invasion and wound-healing assays, it was revealed that the knockdown of AQP9 suppressed astrocytoma cell invasion and motility, whereas overexpression of AQP9 promoted the invasion and motility of astrocytoma cells. It was further revealed that AQP9 could induce RAC serine/threonine-protein kinase (AKT) activation and decrease E-cadherin expression in astrocytoma cells. Inhibition of the AKT pathway attenuated AQP9-mediated invasion, motility and E-cadherin expression. Taken together, the results of the present study indicated that AQP9 promoted the invasion and motility of cells via the AKT pathway. Therefore, AQP9 may represent a potential target for therapeutic use of astrocytoma.

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“…Recent studies have reported that impaired AQP9 expression may contribute to the development of numerous types of cancer, such as lung cancer and malignant brain tumour [16,17]. For instance, the expression of AQP9 in prostate cancer was significantly increased compared with the adjacent tissues [16]. Furthermore, AQP9 could promote the proliferation, migration and invasion, whereas inhibit the apoptosis of prostate cancer cells.…”

Section: Discussionmentioning

confidence: 99%

Aquaporin 9 inhibits growth and metastasis of hepatocellular carcinoma cells via Wnt/β-catenin pathway

Liao

Chen

Liu

et al. 2020

Aging

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Hepatocellular carcinoma (HCC) is the most common type of liver cancer worldwide, and it is the second leading cause of cancer-related mortality. Aquaporin 9 (AQP9) is an essential aquaporin in the liver and located in the basolateral membrane of hepatocytes, but its roles on HCC has not been completely elucidated. This study investigated the regulatory functions of AQP9 in the pathogenesis of HCC. The expression levels of AQP9 were significantly down-regulated in HCC tissues and cells, which was also correlated with tumor size and number, TNM stage, five-year survival rate, lymphatic and distal metastasis within the patients. Furthermore, overexpressed AQP9 suppressed the proliferation, migration and invasion of HCC cells. The levels of PCNA, Ecad, N-cad, α-SMA, DVL2, GSK-3β, cyclinD1 and β-catenin in HCC cells were reduced by overexpressed AQP9, while cell apoptosis was remarkably enhanced. Additionally, following the treatment with Wnt/β-catenin signaling inhibitor (XAV939), the proliferative activity of HCC cells was significantly inhibited; PCNA and EMTrelated markers were down-regulated; migration and invasion of cells were notably suppressed; cell apoptotic rate was decreased. Vice versa, after the cells were treated with Wnt/β-catenin inducer (SKL2001), the effects caused by overexpressed AQP9 were abrogated. In vivo studies indicated that tumor volume and weight were remarkably decreased in AQP9 overexpression group, where the levels of Wnt/β-catenin signaling-and EMTassociated molecules were also reduced. Taken together, our results suggested that overexpressed AQP9 could inhibit growth and metastasis of HCC cells via Wnt/β-catenin pathway. AQP9 may be a promising therapeutic target for the treatment of patients with HCC.

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Effect of AQP9 Expression in Androgen-Independent Prostate Cancer Cell PC3

Cited by 20 publications

References 23 publications

RETRACTED: Long Non-coding RNA LINC00320 Inhibits Tumorigenicity of Glioma Cells and Angiogenesis Through Downregulation of NFKB1-Mediated AQP9

RETRACTED: Long Non-coding RNA LINC00320 Inhibits Tumorigenicity of Glioma Cells and Angiogenesis Through Downregulation of NFKB1-Mediated AQP9

AQP9 promotes astrocytoma cell invasion and motility via the AKT pathway

Aquaporin 9 inhibits growth and metastasis of hepatocellular carcinoma cells via Wnt/β-catenin pathway

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