Evidence map›Paper›PMID 38386237›Full record

ArticleGastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association2024

Killer cell lectin-like receptor G2 facilitates aggressive phenotypes of gastric cancer cells via dual activation of the ERK1/2 and JAK/STAT pathways.

Yuki Ito, Mitsuro Kanda, Masahiro Sasahara, Chie Tanaka, Dai Shimizu, Shinichi Umeda, Yoshikuni Inokawa, Norifumi Hattori, Masamichi Hayashi, Goro Nakayama and 1 more

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In one paragraph

Article in Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association, 2024. 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
2.6field-weighted citation impact, top 10% 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, 11 citations in OpenAlex.

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  6. CDCA4 promotes bladder cancer progression by JAK/STAT signaling pathway.Journal of cancer research and clinical oncology · 2025
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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

11 authors at 1 institution in 1 country.

Yuki ItoDepartment of Gastroenterological Surgery, Nagoya University Graduate School of Medicine, 65 Tsurumai-Cho, Showa-Ku, Nagoya, 466-8550, Japan.
Mitsuro KandaDepartment of Gastroenterological Surgery, Nagoya University Graduate School of Medicine, 65 Tsurumai-Cho, Showa-Ku, Nagoya, 466-8550, Japan. m-kanda@med.nagoya-u.ac.jp.ORCID 0000-0001-5464-3819
Masahiro SasaharaDepartment of Gastroenterological Surgery, Nagoya University Graduate School of Medicine, 65 Tsurumai-Cho, Showa-Ku, Nagoya, 466-8550, Japan.
Chie TanakaDepartment of Gastroenterological Surgery, Nagoya University Graduate School of Medicine, 65 Tsurumai-Cho, Showa-Ku, Nagoya, 466-8550, Japan.
Dai ShimizuDepartment of Gastroenterological Surgery, Nagoya University Graduate School of Medicine, 65 Tsurumai-Cho, Showa-Ku, Nagoya, 466-8550, Japan.
Shinichi UmedaDepartment of Gastroenterological Surgery, Nagoya University Graduate School of Medicine, 65 Tsurumai-Cho, Showa-Ku, Nagoya, 466-8550, Japan.
Yoshikuni InokawaDepartment of Gastroenterological Surgery, Nagoya University Graduate School of Medicine, 65 Tsurumai-Cho, Showa-Ku, Nagoya, 466-8550, Japan.
Norifumi HattoriDepartment of Gastroenterological Surgery, Nagoya University Graduate School of Medicine, 65 Tsurumai-Cho, Showa-Ku, Nagoya, 466-8550, Japan.
Masamichi HayashiDepartment of Gastroenterological Surgery, Nagoya University Graduate School of Medicine, 65 Tsurumai-Cho, Showa-Ku, Nagoya, 466-8550, Japan.
Goro NakayamaDepartment of Gastroenterological Surgery, Nagoya University Graduate School of Medicine, 65 Tsurumai-Cho, Showa-Ku, Nagoya, 466-8550, Japan.
Yasuhiro KoderaDepartment of Gastroenterological Surgery, Nagoya University Graduate School of Medicine, 65 Tsurumai-Cho, Showa-Ku, Nagoya, 466-8550, Japan.
Nagoya University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAdvanced gastric cancer (GC) has a poor prognosis. This study aimed to identify novel GC-related genes as potential therapeutic targets.

methodsKiller cell lectin-like receptor G2 (KLRG2) was identified as a candidate gene by transcriptome analysis of metastatic GC tissues. Small interfering RNA-mediated KLRG2 knockdown in human GC cell lines was used to investigate KLRG2 involvement in signaling pathways and functional behaviors in vitro and in vivo. Clinicopathological data were analyzed in patients stratified according to tumor KLRG2 mRNA expression.

resultsKLRG2 knockdown in GC cells decreased cell proliferation, migration, and invasion; caused cell cycle arrest in G

conclusionsKLRG2 knockdown attenuated the malignant phenotypes of GC cells via downregulation of JAK/STAT and MAPK-ERK1/2 pathway activity and upregulation of p38 MAPK and p53. Targeted suppression of KLRG2 may serve as a new treatment approach for GC.

Indexed as

Janus KinasesStomach NeoplasmsAnimalsCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansMAP Kinase Signaling SystemMicep38 Mitogen-Activated Protein KinasesReceptors, NK Cell Lectin-LikeRNA, MessengerSignal TransductionSTAT Transcription FactorsTumor Suppressor Protein p53Janus Kinasesp38 Mitogen-Activated Protein KinasesReceptors, NK Cell Lectin-LikeRNA, MessengerSTAT Transcription FactorsTumor Suppressor Protein p53Extracellular signal-regulated kinase 1/2Gastric cancerJanus kinase-signal transducer and transcription activatorKiller cell lectin-like receptor G2Xenograft model

Identifiers

PMID38386237
OpenAlexW4392054569

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.