Transcriptional over-expression of chloride intracellular channels 3 and 4 in malignant pleural mesothelioma

Tasiopoulou, Vasiliki S.; Magouliotis, Dimitrios; Solenov, Evgeniy I.; Vavougios, George D.; Molyvdas, Paschalis-Adam; Gourgoulianis, Konstantinos; Hatzoglou, Chrissi; Zarogiannis, Sotirios G.

doi:10.1016/j.compbiolchem.2015.09.012

Cited by 18 publications

(20 citation statements)

References 25 publications

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“…2). It is noted that the relationship between expression level of CLIC3 and prognosis were opposite to the previous reports [13][14][15][16][17], although the types of cancer are different. In fact, expression level of CLIC3 was negatively correlated with pathological tumor depth (Table 1).…”

Section: No Effects Of Clic3 Overexpression On Migration and Invasioncontrasting

confidence: 79%

“…On the other hand, it has been reported that chloride intracellular channel 3 (CLIC3) plays roles as not only a soluble protein, but also an organellar membrane protein [10][11][12]. Moreover, CLIC3 is associated with poor prognosis in pancreatic cancer, breast cancer, ovarian cancer, and malignant pleural mesothelioma [13][14][15][16][17]. Taken together, we have raised two questions: (1) Does CLIC3 act as a Cl − channel in the membrane?, and (2) Page 2 of 11 Kawai et al J Physiol Sci (2020) 70:15 Is CLIC3 expression associated with prognosis of gastric cancer?.…”

Section: Introductionmentioning

confidence: 99%

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Pathophysiological properties of CLIC3 chloride channel in human gastric cancer cells

et al. 2020

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Pathophysiological functions of chloride intracellular channel protein 3 (CLIC3) in human gastric cancer have been unclear. In the tissue microarray analysis using 107 gastric cancer specimens, CLIC3 expression was negatively correlated with pathological tumor depth, and the patients with lower expression of CLIC3 exhibited poorer prognosis. CLIC3 was expressed in the plasma membrane of cancer cells in the tissue. CLIC3 expression was also found in a human gastric cancer cell line (MKN7). In whole-cell patch-clamp recordings of the cells expressing CLIC3, NPPB-sensitive outwardly rectifying Cl − currents were observed. Cell proliferation was significantly accelerated by knockdown of CLIC3 in MKN7 cells. On the other hand, the proliferation was attenuated by exogenous CLIC3 expression in human gastric cancer cells in which endogenous CLIC3 expression is negligible. Our results suggest that CLIC3 functions as a Cl − channel in the plasma membrane of gastric cancer cells and that decreased expression of CLIC3 results in unfavorable prognosis of gastric cancer patients.

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Section: No Effects Of Clic3 Overexpression On Migration and Invasioncontrasting

confidence: 79%

Section: Introductionmentioning

confidence: 99%

Pathophysiological properties of CLIC3 chloride channel in human gastric cancer cells

et al. 2020

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“…A previous study suggested that chloride intracellular channel-4 (CLIC4) exhibit signs of over-expression in tumor types directly associated with cell functions [Peretti et al, 2015]. Down-regulated CLIC4 has been shown much promise proved that could present as a novel treatment approach for various types of cancer [Tasiopoulou et al, 2015].…”

mentioning

confidence: 99%

Retracted: SiRNA‐Mediated Down‐Regulation of CLIC4 Gene Inhibits Cell Proliferation and Accelerates Cell Apoptosis of Mouse Liver Cancer Hca‐F and Hca‐P Cells

Zhou

Xia

et al. 2017

J of Cellular Biochemistry

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This study explored the effects involved in silencing CLIC4 on apoptosis and proliferation of mouse liver cancer Hca-F and Hca-P cells. A CLIC4-target small interfering RNA (siRNA) was designed to compound into two individual complementary oligonucleotide chains. A process of annealing and connection to a pSilencer vector was followed by transfection with Hca-F and Hca-P cells. Quantitative real-time polymerase chain reaction and Western blotting techniques were used to determine CLIC4 mRNA and protein expressions. CCK8 assay and flow cytometry were employed for analysis of the survival and apoptosis rate as well as the cell cycle in an octreotide-induced apoptosis model. Expressions of caspase 3, caspase 9, and cleaved PARP were measured using Western blotting. The CLIC4 mRNA and protein expressions in Hca-F and Hca-P cells transfected by pSilencer-CLIC4 siRNA plasmid in the blank group displayed remarkably decreased levels of expression, when compared with both the control and negative control (NC) groups. Decreased survival rates and cleaved PARP expression, increased cell apoptosis rate, expressions of caspase 3 and caspase 9 in Hca-F and Hca-P cells were detected in groups that had been cultured in a medium containing octreotide. The pSilencer-CLIC4 siRNA-2 group when compared with the control and NC groups exhibited decreased survival rates, cleaved PARP expression, increased cell apoptosis rates, and increased expressions of caspase 3 and caspase 9 of Hca-F and Hca-P cells. The results demonstrated that siRNA-induced down-regulation of CLIC4 could proliferation, while in turn promoting apoptosis of mouse liver cancer Hca-F and Hca-P cells.

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“…In this study we used established data mining techniques through which we have already reported AQP1, CLIC3, CLIC4 , and BBS1 to be ideal candidates for further study in MPM pathophysiology (Jagirdar et al, 2013; Tasiopoulou et al, 2015; Vavougios et al, 2015). …”

Section: Discussionmentioning

confidence: 99%

Transcriptomic Analysis of the Claudin Interactome in Malignant Pleural Mesothelioma: Evaluation of the Effect of Disease Phenotype, Asbestos Exposure, and CDKN2A Deletion Status

et al. 2017

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Malignant pleural mesothelioma (MPM) is a highly aggressive tumor primarily associated with asbestos exposure. Early detection of MPM is restricted by the long latency period until clinical presentation, the ineffectiveness of imaging techniques in early stage detection and the lack of non-invasive biomarkers with high sensitivity and specificity. In this study we used transcriptome data mining in order to determine which CLAUDIN (CLDN) genes are differentially expressed in MPM as compared to controls. Using the same approach we identified the interactome of the differentially expressed CLDN genes and assessed their expression profile. Subsequently, we evaluated the effect of tumor histology, asbestos exposure, CDKN2A deletion status, and gender on the gene expression level of the claudin interactome. We found that 5 out of 15 studied CLDNs (4, 5, 8, 10, 15) and 4 out of 27 available interactors (S100B, SHBG, CDH5, CXCL8) were differentially expressed in MPM specimens vs. healthy tissues. The genes encoding the CLDN-15 and S100B proteins present differences in their expression profile between the three histological subtypes of MPM. Moreover, CLDN-15 is significantly under-expressed in the cohort of patients with previous history of asbestos exposure. CLDN-15 was also found significantly underexpressed in patients lacking the CDKN2A gene. These results warrant the detailed in vitro investigation of the role of CDLN-15 in the pathobiology of MPM.

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Transcriptional over-expression of chloride intracellular channels 3 and 4 in malignant pleural mesothelioma

Cited by 18 publications

References 25 publications

Pathophysiological properties of CLIC3 chloride channel in human gastric cancer cells

Pathophysiological properties of CLIC3 chloride channel in human gastric cancer cells

Retracted: SiRNA‐Mediated Down‐Regulation of CLIC4 Gene Inhibits Cell Proliferation and Accelerates Cell Apoptosis of Mouse Liver Cancer Hca‐F and Hca‐P Cells

Transcriptomic Analysis of the Claudin Interactome in Malignant Pleural Mesothelioma: Evaluation of the Effect of Disease Phenotype, Asbestos Exposure, and CDKN2A Deletion Status

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