Evidence map›Paper›PMID 37684371›Full record

ArticleAnnals of surgical oncology2023

Cancer Stem Cells of Esophageal Adenocarcinoma are Suppressed by Inhibitors of TRPV2 and SLC12A2.

Atsushi Shiozaki, Hiroyuki Inoue, Hiroki Shimizu, Toshiyuki Kosuga, Kenichi Takemoto, Michihiro Kudou, Takuma Ohashi, Tomohiro Arita, Hirotaka Konishi, Shuhei Komatsu and 3 more

Abstract read
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Article in Annals of surgical oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.4field-weighted citation impact, top 16% 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

6 citing papers in PubMed, 6 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 1 institution in 1 country.

Atsushi Shiozaki *Division of Digestive Surgery, Department of Surgery, Kyoto Prefectural University of Medicine, Kyoto, Japan. shiozaki@koto.kpu-m.ac.jp.ORCID http://orcid.org/0000-0003-3739-160X
Hiroyuki Inoue *Division 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.
Toshiyuki KosugaDivision of Digestive Surgery, Department of Surgery, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Kenichi TakemotoDivision of Digestive Surgery, Department of Surgery, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Michihiro KudouDivision of Digestive Surgery, Department of Surgery, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Takuma OhashiDivision 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.
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.
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 Grants-in-Aid for Scientific Research (C) 20K09016Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research (C) 20K09084Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research (C) 21K08689Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research (C) 22K08832Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research (C) 23K06654Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research (C) 23K08115Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research (C) 23K08218Japan Society for the Promotion of Science Grants-in-Aid for Young Scientists 20K17659Japan Society for the Promotion of Science Grants-in-Aid for Young Scientists 21K16456Japan Society for the Promotion of Science Grants-in-Aid for Young Scientists 22K16518
6 · The paper itself

Abstract

backgroundThe potential of membrane transporters activated in cancer stem cells (CSCs) as new therapeutic targets for cancer is attracting increasing interest. Therefore, the present study examined the expression profiles of ion transport-related molecules in the CSCs of esophageal adenocarcinoma (EAC).

methodsCells that highly expressed aldehyde dehydrogenase 1 family member A1 (ALDH1A1) were separated from OE33 cells, a human Barrett's EAC cell line, by fluorescence-activated cell sorting. CSCs were identified based on the formation of tumorspheres. Gene expression profiles in CSCs were examined by a microarray analysis.

resultsAmong OE33 cells, ALDH1A1 messenger RNA levels were higher in CSCs than in non-CSCs. Furthermore, CSCs exhibited resistance to cisplatin and had the capacity to redifferentiate. The results of the microarray analysis of CSCs showed the up-regulated expression of several genes related to ion channels/transporters, such as transient receptor potential vanilloid 2 (TRPV2) and solute carrier family 12 member 2 (SLC12A2). The cytotoxicities of the TRPV2 inhibitor tranilast and the SLC12A2 inhibitor furosemide were higher at lower concentrations in CSCs than in non-CSCs, and both markedly reduced the number of tumorspheres. The cell population among OE33 cells that highly expressed ALDH1A1 also was significantly decreased by these inhibitors.

conclusionsBased on the present results, TRPV2 and SLC12A2 are involved in the maintenance of CSCs, and their specific inhibitors, tranilast and furosemide, respectively, have potential as targeted therapeutic agents for EAC.

Indexed as

AdenocarcinomaAntineoplastic AgentsEsophageal NeoplasmsCell Line, TumorFurosemideHumansNeoplastic Stem Cellsortho-AminobenzoatesSolute Carrier Family 12, Member 2TRPV Cation ChannelsAntineoplastic AgentsFurosemideortho-AminobenzoatesSLC12A2 protein, humanSolute Carrier Family 12, Member 2tranilastTRPV2 protein, humanTRPV Cation ChannelsCancer stem cellEsophageal adenocarcinomaFurosemideSLC12A2TranilastTRPV2

Identifiers

PMID37684371
OpenAlexW4386533689

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.