Nasopharyngeal carcinoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
The ClC-3 chloride channel protein is a downstream target of cyclin D1 in nasopharyngeal carcinoma cells.
|
23270726 |
2013 |
Nasopharyngeal carcinoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
ClC-3 protein may be considered as a potential tumor marker and therapeutic target for human nasopharyngeal carcinoma.
|
22108225 |
2012 |
Nasopharyngeal carcinoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
ClC-3 may regulate CNE-2Z cell migration by modulating cell volume.
|
18359479 |
2008 |
Nasopharyngeal carcinoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
Nevertheless, ClC-3 knockdown had little effect on ROS levels, indicating that ROS acted upstream of ClC-3 and that both ROS and ClC-3 participated in EBSS-induced autophagy regulation in CNE-2Z.
|
30992317 |
2019 |
Nasopharyngeal carcinoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
The AQP-3 water channel and the ClC-3 chloride channel coordinate the hypotonicity-induced swelling volume in nasopharyngeal carcinoma cells.
|
25450461 |
2014 |
Nasopharyngeal carcinoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
ClC-3 is a candidate of the channel proteins that mediate or regulate the acid-activated chloride current in nasopharyngeal carcinoma cells.
|
22496242 |
2012 |
Nasopharyngeal carcinoma
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
ClC-3 is a main component of background chloride channels activated under isotonic conditions by autocrine ATP in nasopharyngeal carcinoma cells.
|
21792908 |
2011 |
Nasopharyngeal carcinoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
We previously reported that AQP-3 aquaglyceroporin and ClC-3 chloride channels could form complexes to regulate cell volume in nasopharyngeal carcinoma cells.
|
26794461 |
2016 |
Nasopharyngeal carcinoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
Here, we showed that the involvement of ClC-3 chloride channel in the selective cytotoxicity of DSF/Cu<sup>2+</sup> in the poorly-differentiated nasopharyngeal carcinoma.
|
31606620 |
2019 |
Nasopharyngeal carcinoma
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Our data demonstrated that the selective antitumor activities of DHA in NPC may occur through the specific activation of the CLC-3 Cl<sup>-</sup> channel, leading to Cl<sup>-</sup> efflux, and induced AVD, then led to [Ca<sup>2+</sup> ]<sub>i</sub> accumulation and caspase-3 activation, and finally induced apoptosis.
|
30171707 |
2018 |
Glioma
|
0.340 |
AlteredExpression
|
disease |
BEFREE |
Suppression of chloride channel 3 expression facilitates sensitivity of human glioma U251 cells to cisplatin through concomitant inhibition of Akt and autophagy.
|
23408563 |
2013 |
Glioma
|
0.340 |
Biomarker
|
disease |
BEFREE |
Taken together, these results suggest CLC-3 promotes the aggressiveness of glioma at least in part through nuclear factor-κB pathway, and might be a novel prognostic biomarker and therapeutic target for glioma.
|
28969029 |
2017 |
Glioma
|
0.340 |
Biomarker
|
disease |
BEFREE |
Therefore, the present study explored the involvement of CLCN3 in cisplatin resistance in human glioma U251 cells.
|
29963152 |
2018 |
Glioma
|
0.340 |
Biomarker
|
disease |
BEFREE |
In the present study we provide several lines of evidence that glioma Cl- currents are primarily mediated by ClC-2 and ClC-3, two genes that belong to the ClC superfamily.
|
12843258 |
2003 |
Malignant neoplasm of stomach
|
0.320 |
Biomarker
|
disease |
BEFREE |
The molecular mechanisms by which CLC-3 is regulated in GC are unclear.
|
30217218 |
2018 |
Malignant neoplasm of stomach
|
0.320 |
Biomarker
|
disease |
BEFREE |
These findings indicate the vital role of CLC-3 in gastric cancer progression and its potential role of a therapeutic target for treatment.
|
29795988 |
2018 |
Neuronal Ceroid-Lipofuscinoses
|
0.210 |
Biomarker
|
disease |
BEFREE |
These results indicated that the neurodegeneration observed in the Clcn3-/- mice was caused by an abnormality in the machinery which degrades the cellular protein and was associated with the phenotype of neuronal ceroid lipofuscinosis (NCL).
|
12059962 |
2002 |
Schizophrenia
|
0.110 |
GeneticVariation
|
disease |
BEFREE |
By integrating CRISPR-mediated gene editing, activation and repression technologies to study one putative SZ eQTL (FURIN rs4702) and four top-ranked SZ eQTL genes (FURIN, SNAP91, TSNARE1 and CLCN3), our platform resolves pre- and postsynaptic neuronal deficits, recapitulates genotype-dependent gene expression differences and identifies convergence downstream of SZ eQTL gene perturbations.
|
31548722 |
2019 |
Neoplasms
|
0.070 |
Biomarker
|
group |
BEFREE |
Chloride channel-3 (CLC-3) has been reported to promote the proliferation and invasion in various tumors, yet little is known about its role in gastric cancer.
|
29795988 |
2018 |
Neoplasms
|
0.070 |
AlteredExpression
|
group |
BEFREE |
The expression level of ClC-3 was closely-related to the histological differentiation (p = 0.029), tumour staging (<i>p </i>= 0.016), tumour size (<i>p </i>= 0.039), vascular invasion (<i>p </i>= 0.045), interstitial infiltration depth (<i>p </i>= 0.012), lymphatic metastasis (<i>p </i>= 0.036), and HPV infection (<i>p </i>= 0.022).
|
30636929 |
2019 |
Neoplasms
|
0.070 |
AlteredExpression
|
group |
BEFREE |
BACKGROUND Recently, ClC-3 chloride channel expression has been noted to be high in some tumors.
|
31281178 |
2019 |
Neoplasms
|
0.070 |
Biomarker
|
group |
BEFREE |
ClC-3 is a type of chloride channel that has multiple functions in tumorigenesis and tumor growth, and can be blocked by DIDS (4,4'-diisothiocyanostilbene-2,2'-disulfonic acid).
|
29749557 |
2018 |
Neoplasms
|
0.070 |
AlteredExpression
|
group |
BEFREE |
Moreover, up-regulation of CIC-3 markedly correlated with tumor size and overall prognosis, suggesting that CIC-3 expression could predict both tumor size and overall prognosis in hepatocarcinoma.
|
30678806 |
2019 |
Neoplasms
|
0.070 |
AlteredExpression
|
group |
BEFREE |
Chloride channel-3 (ClC-3) is over-expressed in a variety of cancers and involves multiple tumor biological events.
|
31606620 |
2019 |
Neoplasms
|
0.070 |
Biomarker
|
group |
BEFREE |
Together, our data suggest that upregulation of ClC-3 by IGF-1 contributes to cell proliferation and tumor growth in breast cancer, and ClC-3 deficiency suppresses cell proliferation and tumor growth via the IGF/IGF receptor/ERK pathway.
|
29963105 |
2018 |