Evidence map›Paper›PMID 34855108›Full record

ArticleMolecular biology reports2022

Interferon-induced transmembrane protein 2 promotes epithelial-mesenchymal transition by activating transforming growth factor-β1/small mother against decapentaplegic 2 signaling in gastric cancer.

Yonggang Liu, Minyu Zhou, Jianhua Wu, Zhaowei Wen, Yisheng Fang, Li Lin, Meihua Luo, Li Sun, Wangjun Liao

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In one paragraph

Article in Molecular biology reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.6field-weighted citation impact, top 39% 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

9 citing papers in PubMed, 10 citations in OpenAlex.

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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

9 authors at 2 institutions in 1 country.

Yonggang LiuDepartment of Oncology, Nanfang Hospital, Southern Medical University, No. 1838 Guangzhou Avenue North, Guangzhou, 510515, Guangdong, China.ORCID http://orcid.org/0000-0002-8486-6332
Minyu ZhouDepartment of Oncology, Nanfang Hospital, Southern Medical University, No. 1838 Guangzhou Avenue North, Guangzhou, 510515, Guangdong, China.
Jianhua WuDepartment of Oncology, Nanfang Hospital, Southern Medical University, No. 1838 Guangzhou Avenue North, Guangzhou, 510515, Guangdong, China.
Zhaowei WenDepartment of Oncology, Nanfang Hospital, Southern Medical University, No. 1838 Guangzhou Avenue North, Guangzhou, 510515, Guangdong, China.
Yisheng FangDepartment of Oncology, Nanfang Hospital, Southern Medical University, No. 1838 Guangzhou Avenue North, Guangzhou, 510515, Guangdong, China.
Li LinDepartment of Oncology, Nanfang Hospital, Southern Medical University, No. 1838 Guangzhou Avenue North, Guangzhou, 510515, Guangdong, China.
Meihua LuoDepartment of Oncology, Shunde Hospital, Southern Medical University, (The First People's Hospital of Shunde), Foshan, 528308, Guangdong, China.
Li SunDepartment of Oncology, Nanfang Hospital, Southern Medical University, No. 1838 Guangzhou Avenue North, Guangzhou, 510515, Guangdong, China. sunlishining@163.com.
Wangjun LiaoDepartment of Oncology, Nanfang Hospital, Southern Medical University, No. 1838 Guangzhou Avenue North, Guangzhou, 510515, Guangdong, China. nfyyliaowj@163.com.
Nanfang Hospital · CNThe First People's Hospital of Shunde · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGastric cancer (GC) is one of the most prevalent malignancy around the world. Primary tumor cells are enabled to invade and migrate into adjacent normal tissues to form secondary tumors. Epithelial-mesenchymal transitions (EMT) plays a pivotal role in facilitating tumor progression. Abundant evidence suggested that the transforming growth factor-β1 (TGF-β1) triggered the process of EMT. Nonetheless, the precise molecular mechanisms underlying EMT requires further elucidation, and there still lacks effective specific therapeutic target. In our recent research, we demonstrated that the interferon (IFN)-induced transmembrane protein 2 (IFITM2) promoted the growth and metastasis of GC. However, it remains unclear whether IFITM2 involves in TGF-β1 mediated EMT in GC. METHODS AND

resultsIn the present research, we investigated the functional role of IFITM2 in EMT process and TGF-β1 signaling pathway in two GC cell lines. We noticed that silencing IFITM2 can effectively inhibit TGF-β1 signaling mediated EMT by regulating down stream small mother against decapentaplegic (SMAD) 2/3 and transcription factors.This finding was further determined in both tumor tissues from GC patients and normal tissues adjacent to cancer. Our data demonstrated the key role of IFITM2 in TGF-β1 signaling and EMT in GC.

conclusionThe findings enriched our understanding of the underlying mechanism in EMT during the progression of GC. In addition, IFITM2 would be a potential target for treating GC and other malignant tumors.

Indexed as

Cell Line, TumorCell MovementChinaDatabases, GeneticEpithelial-Mesenchymal TransitionGene ExpressionGene Expression Regulation, NeoplasticHumansInterferonsMembrane ProteinsSignal TransductionSmad2 ProteinStomach NeoplasmsTranscription FactorsTransforming Growth Factor beta1IFITM2 protein, humanInterferonsMembrane ProteinsSmad2 ProteinSMAD2 protein, humanTGFB1 protein, humanTranscription FactorsTransforming Growth Factor beta1Cancer invasion and metastasisEpithelial-mesenchymal transitionsGastric cancerIFITM2Molecular mechanismTGF-β1

Identifiers

PMID34855108
OpenAlexW3217677552

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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.