Evidence map›Paper›PMID 33565032›Full record

ArticleAnnals of surgical oncology2021

Functional Analysis and Clinical Significance of Chloride Channel 2 Expression in Esophageal Squamous Cell Carcinoma.

Masato Mitsuda, Atsushi Shiozaki, Michihiro Kudou, Hiroki Shimizu, Tomohiro Arita, Toshiyuki Kosuga, Hirotaka Konishi, Shuhei Komatsu, Takeshi Kubota, Hitoshi Fujiwara and 4 more

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Article in Annals of surgical oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.6field-weighted citation impact, top 37% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Article
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  4. Physiological roles of chloride ions in bodily and cellular functions.The journal of physiological sciences : JPS · 2023
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 1 institution in 1 country.

Masato Mitsuda *Division of Digestive Surgery, Department of Surgery, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Atsushi Shiozaki *Division of Digestive Surgery, Department of Surgery, Kyoto Prefectural University of Medicine, Kyoto, Japan. shiozaki@koto.kpu-m.ac.jp.
Michihiro KudouDivision of Digestive Surgery, Department of Surgery, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Hiroki ShimizuDivision of Digestive Surgery, Department of Surgery, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Tomohiro AritaDivision of Digestive Surgery, Department of Surgery, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Toshiyuki KosugaDivision of Digestive Surgery, Department of Surgery, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Hirotaka KonishiDivision of Digestive Surgery, Department of Surgery, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Shuhei KomatsuDivision of Digestive Surgery, Department of Surgery, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Takeshi KubotaDivision of Digestive Surgery, Department of Surgery, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Hitoshi FujiwaraDivision of Digestive Surgery, Department of Surgery, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Kazuma OkamotoDivision of Digestive Surgery, Department of Surgery, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Mitsuo KishimotoDepartment of Pathology, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Eiichi KonishiDepartment of Pathology, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Eigo OtsujiDivision of Digestive Surgery, Department of Surgery, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Kyoto Prefectural University of Medicine · JP

Funding

Japan Society for the Promotion of Science 17K10710Japan Society for the Promotion of Science 18K08628Japan Society for the Promotion of Science 18K08689Japan Society for the Promotion of Science 19K09182Japan Society for the Promotion of Science 19K09202Japan Society for the Promotion of Science Grant-in-Aid for Young Scientists/ 19K18160Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research/ 17K10602
6 · The paper itself

Abstract

backgroundChloride channel 2 (CLCN2) was recently shown to affect tumor behavior. The present study examined the functions of CLCN2 in the regulation of genes that play a role in tumor progression, as well as its clinicopathological significance in esophageal squamous cell carcinoma (ESCC).

methodsKnockdown experiments were conducted using CLCN2-small-interfering RNA, and changes in proliferation, survival, and cellular movement in human ESCC cell lines were investigated. A microarray analysis of gene expression profiles in CLCN2-depleted ESCC cells was conducted. Fifty-four primary ESCC samples were examined by immunohistochemistry (IHC).

resultsThe strong expression of CLCN2 was detected in TE5 and KYSE70 cells. Downregulated expression of CLCN2 enhanced proliferation and decreased apoptosis, whereas its upregulation inhibited proliferation and increased apoptosis. The effects of lubiprostone, a CLCN2 activator, were also investigated. In lubiprostone-treated cells, proliferation was inhibited and apoptosis was increased. The microarray analysis demonstrated that interferon (IFN) signaling-related genes were downregulated in CLCN2-depleted cells. IHC showed the presence of CLCN2 in the cytoplasm and cell membranes of ESCC cells. The prognostic analysis revealed a relationship between weak CLCN2 expression and shorter overall survival.

conclusionsThe present results indicate that tumor progression is regulated by CLCN2 through its effects on IFN signaling. Furthermore, weak CLCN2 expression was associated with poorer outcomes in ESCC patients. The present study will contribute to a clearer understanding of the role of CLCN2 as a mediator of ESCC, as well as its use as a biomarker for this cancer.

Indexed as

Carcinoma, Squamous CellEsophageal NeoplasmsEsophageal Squamous Cell CarcinomaHead and Neck NeoplasmsApoptosisBiomarkers, TumorCell Line, TumorCell MovementCell ProliferationChloride ChannelsCLC-2 Chloride ChannelsGene Expression Regulation, NeoplasticHumansPrognosisBiomarkers, TumorChloride ChannelsCLC-2 Chloride Channels

Identifiers

PMID33565032
OpenAlexW3126895516

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.