Evidence map›Paper›PMID 35151264›Full record

ArticleBMC cancer2022

SYT-SSX1 enhances the invasiveness and maintains stem-like cell properties in synovial sarcoma via induction of TGF-β1/Smad signaling.

Yan Qi, Shuang-Shuang Dong, Yong-Lai He, Zi-Han Liu, Ya-Lan Huang, Ning Wang, Zhen Zhang, Zhong Li, Mei Er Tu He Ta Mi Shi, Xiao Feng and 5 more

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
1.7field-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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.

  1. Pooled it
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  10. Cancer/Testis Antigens as Targets for RNA-Based Anticancer Therapy.International journal of molecular sciences · 2023
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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

15 authors at 6 institutions in 1 country.

Yan Qi *Department of Pathology, Central People's Hospital of Zhanjiang & Zhanjiang Central Hospital, Guangdong Medical University, Zhanjiang, Guangdong, 524000, China. qiyanyan-1998@163.com.
Shuang-Shuang Dong *Department of Pathology, Shihezi University School of Medicine & the First Affiliated Hospital to Shihezi University School of Medicine, North 2 road, Shihezi, Xinjiang, 832002, China.
Yong-Lai He *Department of ICU, Central People's Hospital of Zhanjiang & Zhanjiang Central Hospital, Guangdong Medical University, Zhanjiang, Guangdong, 524000, China.
Zi-Han LiuDepartment of Pathology, The Affiliated Hospital of Qingdao university, Qingdao, China.
Ya-Lan HuangDepartment of Pathology, Suining Central Hospital, Suining, Sichuan, China.
Ning WangDepartment of Pathology, Shihezi University School of Medicine & the First Affiliated Hospital to Shihezi University School of Medicine, North 2 road, Shihezi, Xinjiang, 832002, China.
Zhen ZhangDepartment of Pathology, Shihezi University School of Medicine & the First Affiliated Hospital to Shihezi University School of Medicine, North 2 road, Shihezi, Xinjiang, 832002, China.
Zhong LiDepartment of Pathology, Shihezi University School of Medicine & the First Affiliated Hospital to Shihezi University School of Medicine, North 2 road, Shihezi, Xinjiang, 832002, China.
Mei Er Tu He Ta Mi ShiDepartment of Pathology, Shihezi University School of Medicine & the First Affiliated Hospital to Shihezi University School of Medicine, North 2 road, Shihezi, Xinjiang, 832002, China.
Xiao FengDepartment of Pathology, Shihezi University School of Medicine & the First Affiliated Hospital to Shihezi University School of Medicine, North 2 road, Shihezi, Xinjiang, 832002, China.
Qing YaoDepartment of Pathology, Shihezi University School of Medicine & the First Affiliated Hospital to Shihezi University School of Medicine, North 2 road, Shihezi, Xinjiang, 832002, China.
Hong ZouDepartment of Pathology, Shihezi University School of Medicine & the First Affiliated Hospital to Shihezi University School of Medicine, North 2 road, Shihezi, Xinjiang, 832002, China.
Jian-Ming HuDepartment of Pathology, Shihezi University School of Medicine & the First Affiliated Hospital to Shihezi University School of Medicine, North 2 road, Shihezi, Xinjiang, 832002, China.
Li-Juan PangDepartment of Pathology, Shihezi University School of Medicine & the First Affiliated Hospital to Shihezi University School of Medicine, North 2 road, Shihezi, Xinjiang, 832002, China.
Feng LiDepartment of Pathology, Shihezi University School of Medicine & the First Affiliated Hospital to Shihezi University School of Medicine, North 2 road, Shihezi, Xinjiang, 832002, China. lifeng7855@126.com.
Shihezi University · CNAffiliated Hospital of Qingdao University · CNCapital Medical University · CNCentral People's Hospital of Zhanjiang · CNGuangdong Medical College · CNSuizhou Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSynovial sarcoma (SS) is a type of soft tissue sarcoma (STS) of undetermined tissue origin, which is characterized by the recurrent pathognomonic chromosomal translocation t (X;18)(p11.2; q11.2). Studies have shown that SS is a malignant tumor originating from cancer stem cells or pluripotent mesenchymal stem cells and may be related to fusion genes. In addition, some studies have indicated that the induction of epithelial-mesenchymal transition (EMT) via the TGF-β1/Smad signaling pathway leads to SS metastasis.

methodsWe analyzed the effects of SYT-SSX1 on the stemness of SS cells via TGF-β1/Smad signaling in vitro. The SYT-SSX1 fusion gene high expression cell was constructed by lentiviral stable transfer technology. SYT-SSX1 and SW982 cells were cultured and tested for sphere-forming ability. The transwell migration assay and flow cytometry were used to assess the migration ability of the sphere cells as well as the expression of CSC-related markers. We treated SYT-SSX1 cells with rhTGF-β1 (a recombinant agent of the TGF-β1 signaling pathway) and SB431542 and observed morphological changes. A CCK-8 experiment and a western blot (WB) experiment were conducted to detect the expression of TGF-β1 signaling pathway- and EMT-related proteins after treatment. The SYT-SSX1 cells were then cultured and their ability to form spheres was tested. Flow cytometry, WB, and quantitative real-time polymerase chain reaction (qRT-PCR) were used to detect the expression of CSC surface markers on SYT-SSX1 sphere cells.

resultsIt was found that SYT-SSX1 has stronger sphere-forming ability, migration ability, and higher expression of CSC-related molecules than SW982 cells. Through treating SYT-SSX1 and SW982 cells with rhTGF-β1 and SB431542, we found that TGF-β1 enhanced the proliferation of cells, induced EMT, and that TGF-β1 enhanced the characteristics of tumor stem cells.

conclusionsOur results suggest that SYT-SSX1 enhances invasiveness and maintains stemness in SS cells via TGF-β1/Smad signaling. These findings reveal an effective way to potentially improve the prognosis of patients with SS by eliminating the characteristics of cancer stem cells (CSCs) during treatment.

Indexed as

Biomarkers, TumorCell Line, TumorEpithelial-Mesenchymal TransitionHumansNeoplasm InvasivenessOncogene Proteins, FusionPrognosisSarcomaSarcoma, SynovialSignal TransductionSmad ProteinsSoft Tissue NeoplasmsTransforming Growth Factor beta1Translocation, GeneticBiomarkers, TumorOncogene Proteins, FusionSmad ProteinsSYT-SSX fusion proteinTGFB1 protein, humanTransforming Growth Factor beta1Cancer stem cellEpithelial–mesenchymal transitionSignaling pathwaySynovial sarcomaSYT-SSX1TGF-β1/Smad

Identifiers

PMID35151264
PMCPMC8841078
OpenAlexW4211076502

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LicenceCC BY
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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.