ArticleCancer management and research2018
Overexpression of chloride channel-3 predicts unfavorable prognosis and promotes cellular invasion in gastric cancer.
Article in Cancer management and research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 7 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.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- CLC-3 regulates TGF-β/smad signaling pathway to inhibit the process of fibrosis in hypertrophic scar.Heliyon · 2024Article
- Multimodal AI for prediction of distant metastasis in carcinoma patients.Frontiers in bioinformatics · 2023Article
- Hyperglycemia induces miR-26-5p down-regulation to overexpress PFKFB3 and accelerate epithelial-mesenchymal transition in gastric cancer.Bioengineered · 2022Article
- Pathophysiological role of ion channels and transporters in gastrointestinal mucosal diseases.Cellular and molecular life sciences : CMLS · 2021Review
- Pathophysiological properties of CLIC3 chloride channel in human gastric cancer cells.The journal of physiological sciences : JPS · 2020Article
- The role and mechanism of microRNA‑18a‑5p in oral squamous cell carcinoma.Molecular medicine reports · 2019Article
- Hyperglycemia promotes Snail-induced epithelial-mesenchymal transition of gastric cancer via activating ENO1 expression.Cancer cell international · 2019Article
Corrections and comments
- Retraction · 2024-05-16Concerns/Issues about Image · Euphemisms for Plagiarism · Investigation by Journal/Publisher · Plagiarism of Image · Unreliable Results and/or Conclusions ·
- Retracted
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundChloride 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. In the present study, we investigated the clinical significance of CLC-3 and its biological role in gastric cancer.
methodsBioinformatic analysis, immunohistochemical staining, quantitative real-time polymerase chain reaction and Western blot assay were used to assess the expression of CLC-3 and its clinical significance in gastric cancer. The biological role of CLC-3 and its underlying mechanism were detected through in vitro experiments.
resultsCLC-3 was highly expressed in gastric cancer tissues and cell lines, and high levels of CLC-3 were significantly associated with adverse clinicopathological parameters and shorter overall survival time in patients with gastric cancer. Functional studies revealed that silencing of CLC-3 decreased, while overexpression promoted, the proliferation, migration and invasion of gastric cancer cells in vitro. Mechanistic studies suggested that canonical TGF-β/Smad signaling pathway is involved in CLC-3-induced gastric cancer cells proliferation, migration and invasion.
conclusionThese findings indicate the vital role of CLC-3 in gastric cancer progression and its potential role of a therapeutic target for treatment.
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