The ClC-3 chloride channel protein is a downstream target of cyclin D1 in nasopharyngeal carcinoma cells

2013 ◽  
Vol 45 (3) ◽  
pp. 672-683 ◽  
Author(s):  
Haifeng Zhang ◽  
Linyan Zhu ◽  
Wanhong Zuo ◽  
Hai Luo ◽  
Jianwen Mao ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Cyclin D1 ◽  
Chloride Channel ◽  
Carcinoma Cells ◽  
Channel Protein ◽  
Downstream Target

ClC-3 is a candidate of the channel proteins mediating acid-activated chloride currents in nasopharyngeal carcinoma cells

2012 ◽  
Vol 303 (1) ◽  
pp. C14-C23 ◽  
Author(s):  
Liwei Wang ◽  
Wenbo Ma ◽  
Linyan Zhu ◽  
Dong Ye ◽  
Yuan Li ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Chloride Channel ◽  
Cell Function ◽  
Extracellular Ph ◽  
Carcinoma Cells ◽  
Chloride Current ◽  
Disulfonic Acid ◽  
Channel Blockers ◽  
Chloride Currents ◽  
Channel Proteins

Acid-activated chloride currents have been reported in several cell types and may play important roles in regulation of cell function. However, the molecular identities of the channels that mediate the currents are not defined. In this study, activation of the acid-induced chloride current and the possible candidates of the acid-activated chloride channel were investigated in human nasopharyngeal carcinoma cells (CNE-2Z). A chloride current was activated when extracellular pH was reduced to 6.6 from 7.4. However, a further decrease of extracellular pH to 5.8 inhibited the current. The current was weakly outward-rectified and was suppressed by hypertonicity-induced cell shrinkage and by the chloride channel blockers 5-nitro-2–3-phenylpropylamino benzoic acid (NPPB), tamoxifen, and 4,4′-diisothiocyanatostilbene-2,2′-disulfonic acid disodium salt hydrate (DIDS). The permeability sequence of the channel to anions was I− > Br− > Cl− > gluconate−. Among the ClC chloride channels, ClC-3 and ClC-7 were strongly expressed in CNE-2Z cells. Knockdown of ClC-3 expression with ClC-3 small interfering (si)RNA prevented the activation of the acid-induced current, but silence of ClC-7 expression with ClC-7 siRNA did not significantly affect the current. The results suggest that the chloride channel mediating the acid-induced chloride current was volume sensitive. ClC-3 is a candidate of the channel proteins that mediate or regulate the acid-activated chloride current in nasopharyngeal carcinoma cells.

MiR-30a-5p inhibits proliferation, migration and invasion of nasopharyngeal carcinoma cells by targeting NUCB2

2021 ◽  
pp. 096032712199191
Author(s):  
M Li ◽  
Y Wang ◽  
Q Zhao ◽  
W Ma ◽  
J Liu
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Tumor Growth ◽  
Carcinoma Cells ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Binding Interaction ◽  
Downstream Target ◽  
Downstream Target Gene

Background: Nasopharyngeal carcinoma (NPC) is a malignant head and neck tumor arising in the nasopharynx. MicroRNAs (miRNAs) are elucidated to exert tumor-suppressing function in human cancers. Numerous studies have manifested that miR-30a-5p serves as an anti-oncogene in various cancers. Objective: To research the biological function and molecular mechanism of miR-30a-5p in NPC. Methods: The morphology of NPC tissues was revealed by H&E staining. Transwell and wound healing assays were applied to investigate the effects of miR-30a-5p on NPC cell migration. The binding interaction between miR-30a-5p and nucleobindin 2 (NUCB2) was identified by luciferase reporter assay. Xenograft nude mice were used to detect the influence of miR-30a-5p on NPC tumor growth. Results: MiR-30a-5p was downregulated in NPC tissues and cells. The overexpression ofmiR-30a-5p inhibited proliferation, migration and invasion abilities of NPC cells. Moreover, NUCB2 was revealed to be a downstream target gene of miR-30a-5p, and knockdown of NUCB2 repressed the malignant behaviors of NPC cells and tumor growth. Additionally, rescue experiments revealed that miR-30a-5p suppressed the proliferation, migration and invasion of NPC cells via targeting NUCB2 in vitro. Meanwhile, in vivo assays depicted that NUCB2 overexpression rescued the effects induced by miR-30a-5p upregulation on tumor growth. Conclusion: MiR-30a-5p modulates NPC progression by targeting NUCB2. These findings lay a foundation for exploring the clinical treatment of NPC.

scholarly journals Effect of miR-25 on Proliferation of Nasopharyngeal Carcinoma Cells through Wnt/β-Catenin Signaling Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-7
Author(s):  
Haixia He ◽  
Kun Yuan ◽  
Wei Chen
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Cyclin D1 ◽  
Cell Line ◽  
Carcinoma Cell ◽  
Carcinoma Cells ◽  
Carcinoma Cell Line ◽  
Transfected Cells ◽  
Protein Levels ◽  
Qrt Pcr ◽  
Nasopharyngeal Carcinoma Cell

Objective. To investigate the biological role and potential mechanism of miR-25 in nasopharyngeal carcinoma. Methods. The expression of miR-25 in nasopharyngeal carcinoma cell lines was detected by qRT-PCR. The effect of inhibition of miR-25 expression on the proliferative activity of nasopharyngeal carcinoma cell line HONE-1 was examined by CCK-8 method. Flow cytometry was used to detect the effect of miR-25 expression inhibition on the apoptosis rate of nasopharyngeal carcinoma cell line HONE-1. The miRNA target gene prediction site TargetScan predicts the target protein action site of miR-124 and verifies whether miR-25 interacts with the target by luciferase activity assay, qPCR, and Western experiments. The miR-25 inhibitor and target egg gene expression plasmids were cotransfected into HONE-1 cells for rescue experiments to investigate whether miR-25 inhibits proliferation of nasopharyngeal carcinoma cells by target genes. At the same time, qRT-PCR was used to detect the mRNA expression levels of Wnt/β-catenin pathway key proteins TCF4, c-Myc, and Cyclin D1 in different transfected cells. Results. miR-25 expression was upregulated in nasopharyngeal carcinoma cell lines. Functional studies showed that inhibition of miR-25 expression significantly inhibited the proliferation of nasopharyngeal carcinoma cell line HONE-1 ( p < 0.05 ). Inhibition of miR-25 expression by flow cytometry significantly promoted apoptosis ( p < 0.05 ). Detection of dual luciferase activity indicated that DKK3 is a direct target site for miR-25. Western blots showed that inhibition of miR-25 significantly upregulated DKK3 mRNA and protein levels. Supplementation with DKK3 significantly attenuated the inhibitory effect of miR-25 on the proliferation of nasopharyngeal carcinoma cell line HONE-1 ( p < 0.05 ). qRT-PCR found that mRNA levels of TCF4, c-Myc, and Cyclin D1 were significantly upregulated in miR-25-transfected cells compared to control transfection. QRT PCR showed that the mRNA and protein levels of Tcf4, c-myc, and Cyclin D1 were significantly upregulated in miR-25 overexpression-transfected cells. Conclusion. Inhibition of miR-25 expression promotes DKK3 gene expression, and inactivation of Wnt/β-catenin signaling pathway inhibits proliferation and promotes apoptosis of nasopharyngeal carcinoma cells.

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