Evidence map›Paper›PMID 37443145›Full record

ArticleCell death & disease2023

TM4SF1-AS1 inhibits apoptosis by promoting stress granule formation in cancer cells.

Hiroshi Kitajima, Reo Maruyama, Takeshi Niinuma, Eiichiro Yamamoto, Akira Takasawa, Kumi Takasawa, Kazuya Ishiguro, Akihiro Tsuyada, Ryo Suzuki, Gota Sudo and 13 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
6.7field-weighted citation impact, top 3% 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

21 citing papers in PubMed, 28 citations in OpenAlex.

  1. The Role of Long Noncoding RNAs in Modulation of Stress Granules in Cancer.Journal of cellular and molecular medicine · 2026
    Review
  2. Review
  3. The Role of Stress Granules in Cardiovascular Diseases.Reviews in cardiovascular medicine · 2026
    Review
  4. Article
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  7. Review
  8. Stress Granules: Novel Regulators of Programmed Cell Death.Mini reviews in medicinal chemistry · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

23 authors at 2 institutions in 1 country.

Hiroshi Kitajima *Department of Molecular Biology, Sapporo Medical University School of Medicine, Sapporo, Japan.ORCID 0000-0002-7508-6764
Reo Maruyama *Project for Cancer Epigenomics, Cancer Institute, Japanese Foundation for Cancer Research, Tokyo, Japan.
Takeshi NiinumaDepartment of Molecular Biology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Eiichiro YamamotoDepartment of Molecular Biology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Akira TakasawaDepartment of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Kumi TakasawaDepartment of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Kazuya IshiguroDepartment of Molecular Biology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Akihiro TsuyadaDepartment of Molecular Biology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Ryo SuzukiDepartment of Gastroenterology and Hepatology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Gota SudoDepartment of Gastroenterology and Hepatology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Toshiyuki KuboDepartment of Gastroenterology and Hepatology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Kei MitsuhashiDepartment of Gastroenterology and Hepatology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Masashi IdogawaDepartment of Medical Genome Sciences, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan.ORCID 0000-0002-8507-1726
Shoichiro TangeDepartment of Medical Genome Sciences, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan.
Mutsumi ToyotaDepartment of Molecular Biology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Ayano YoshidoDepartment of Molecular Biology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Kohei KumegawaCancer Cell Diversity Project, NEXT-Ganken Program, Japanese Foundation for Cancer Research, Tokyo, Japan.ORCID 0000-0003-3732-2874
Masahiro KaiDepartment of Molecular Biology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Kazuyoshi YanagiharaDivision of Rare Cancer Research, National Cancer Center Research Institute, Tokyo, Japan.
Takashi TokinoDepartment of Medical Genome Sciences, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan.
Makoto OsanaiDepartment of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Hiroshi NakaseDepartment of Gastroenterology and Hepatology, Sapporo Medical University School of Medicine, Sapporo, Japan.ORCID 0000-0003-2848-6586
Hiromu SuzukiDepartment of Molecular Biology, Sapporo Medical University School of Medicine, Sapporo, Japan. hsuzuki@sapmed.ac.jp.ORCID 0000-0001-9635-3238
Sapporo Medical University · JPJapanese Foundation For Cancer Research · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long noncoding RNAs (lncRNAs) play pivotal roles in tumor development. To identify dysregulated lncRNAs in gastric cancer (GC), we analyzed genome-wide trimethylation of histone H3 lysine 4 (H3K4me3) to screen for transcriptionally active lncRNA genes in the non-tumorous gastric mucosa of patients with GC and healthy individuals. We found that H3K4me3 at TM4SF1-AS1 was specifically upregulated in GC patients and that the expression of TM4SF1-AS1 was significantly elevated in primary and cultured GC cells. TM4SF1-AS1 contributes to GC cell growth in vitro and in vivo, and its oncogenic function is mediated, at least in part, through interactions with purine-rich element-binding protein α (Pur-α) and Y-box binding protein 1 (YB-1). TM4SF1-AS1 also activates interferon signaling in GC cells, which is dependent on Pur-α and RIG-I. Chromatin isolation by RNA purification (ChIRP)-mass spectrometry demonstrated that TM4SF1-AS1 was associated with several stress granule (SG)-related proteins, including G3BP2, RACK1, and DDX3. Notably, TM4SF1-AS1 promoted SG formation and inhibited apoptosis in GC cells by sequestering RACK1, an activator of the stress-responsive MAPK pathway, within SGs. TM4SF1-AS1-induced SG formation and apoptosis inhibition are dependent on Pur-α and YB-1. These findings suggested that TM4SF1-AS1 contributes to tumorigenesis by enhancing SG-mediated stress adaptation.

Indexed as

MicroRNAsRNA, Long NoncodingStomach NeoplasmsAntigens, SurfaceApoptosisCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansNeoplasm ProteinsStress GranulesAntigens, SurfaceMicroRNAsNeoplasm ProteinsRNA, Long NoncodingTM4SF1 protein, human

Identifiers

PMID37443145
PMCPMC10345132
OpenAlexW4384199223

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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.