ArticleOncology letters2018
Suppression of chloride voltage-gated channel 3 expression increases sensitivity of human glioma U251 cells to cisplatin through lysosomal dysfunction.
Article in Oncology letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
8 citing papers in PubMed, 8 citations in OpenAlex.
- Targeting lysosomal ion channels to overcome cancer treatment resistance: emerging mechanisms and therapeutic opportunities.Frontiers in pharmacology · 2026Review
- Bioelectricity in dental medicine: a narrative review.Biomedical engineering online · 2024Review
- Ion channels in lung cancer: biological and clinical relevance.Frontiers in pharmacology · 2023Review
- An in vivo genome-wide shRNA screen identifies BCL6 as a targetable biomarker of paclitaxel resistance in breast cancer.Molecular oncology · 2021Article
- Review
- Ion Channels and Their Role in the Pathophysiology of Gliomas.Molecular cancer therapeutics · 2020Review
- Review
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanism of cisplatin resistance is complex. Previous studies have indicated that chloride voltage-gated channel 3 (CLCN3) is associated with drug resistance; however, the mechanisms are not fully understood. Therefore, the present study explored the involvement of CLCN3 in cisplatin resistance in human glioma U251 cells. The effects of combined cisplatin treatment and CLCN3 suppression on cultured U251 cells were investigated. The decreased viability of cisplatin-treated U251 cells indicated the cytotoxic effects of CLCN3 silencing. Expression of the apoptosis-related gene TP53 and caspase 3 activation were enhanced in cisplatin-treated U251 cells. Furthermore, the ratio of BCL2/BAX expression was decreased. Notably, CLCN3 suppression promoted cisplatin-induced cell damage in U251 cells. Thus, the combined use of cisplatin and CLCN3 antisense had additive effects in U251 cells. In addition, the present results indicated that CLCN3 suppression decreased lysosome stabilization in U251 cells treated with cisplatin. To conclude, the present results indicated that CLCN3 suppression can sensitize glioma cells to cisplatin through lysosomal dysfunction.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.