Evidence map›Paper›PMID 26444413›Full record

ArticleJournal of translational medicine2015

SLC39A6: a potential target for diagnosis and therapy of esophageal carcinoma.

Xiao-Bin Cui, Yao-Yuan Shen, Ting-Ting Jin, Su Li, Ting-Ting Li, Shu-Mao Zhang, Hao Peng, Chun-Xia Liu, Shu-Gang Li, Lan Yang and 11 more

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2015. 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
0.8field-weighted citation impact, top 29% 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, 41 citations in OpenAlex.

  1. Article
  2. Review
  3. SpatialESD: Spatial Ensemble Domain Detection in Spatial Transcriptomics.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. The Transcription ofFrontiers in immunology · 2022
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

21 authors at 3 institutions in 2 countries.

Xiao-Bin CuiDepartment of Pathology and Key Laboratory for Xinjiang Endemic and Ethnic Diseases, Shihezi University School of Medicine, North 4th Road, 832002, Shihezi, China. cuixiaobin4363@foxmail.com.
Yao-Yuan ShenDepartment of Pathology and Key Laboratory for Xinjiang Endemic and Ethnic Diseases, Shihezi University School of Medicine, North 4th Road, 832002, Shihezi, China. 491437260@qq.com.
Ting-Ting JinDepartment of Pathology and Key Laboratory for Xinjiang Endemic and Ethnic Diseases, Shihezi University School of Medicine, North 4th Road, 832002, Shihezi, China. 474621590@qq.com.
Su LiDepartment of Pathology and Key Laboratory for Xinjiang Endemic and Ethnic Diseases, Shihezi University School of Medicine, North 4th Road, 832002, Shihezi, China. 944873356@qq.com.
Ting-Ting LiDepartment of Pathology and Key Laboratory for Xinjiang Endemic and Ethnic Diseases, Shihezi University School of Medicine, North 4th Road, 832002, Shihezi, China. 824989630@qq.com.
Shu-Mao ZhangDepartment of Pathology and Key Laboratory for Xinjiang Endemic and Ethnic Diseases, Shihezi University School of Medicine, North 4th Road, 832002, Shihezi, China. 617936327@qq.com.
Hao PengDepartment of Pathology and Key Laboratory for Xinjiang Endemic and Ethnic Diseases, Shihezi University School of Medicine, North 4th Road, 832002, Shihezi, China. 334672404@qq.com.
Chun-Xia LiuDepartment of Pathology and Key Laboratory for Xinjiang Endemic and Ethnic Diseases, Shihezi University School of Medicine, North 4th Road, 832002, Shihezi, China. 342682442@qq.com.
Shu-Gang LiDepartment of Pathology and Key Laboratory for Xinjiang Endemic and Ethnic Diseases, Shihezi University School of Medicine, North 4th Road, 832002, Shihezi, China. 251068648@qq.com.
Lan YangDepartment of Pathology and Key Laboratory for Xinjiang Endemic and Ethnic Diseases, Shihezi University School of Medicine, North 4th Road, 832002, Shihezi, China. yl-branda@163.com.
Na LiDepartment of Oncology, The First Affiliated Hospital, Shihezi University School of Medicine, 832002, Shihezi, China. 1500921245@qq.com.
Jian-Ming HuDepartment of Pathology and Key Laboratory for Xinjiang Endemic and Ethnic Diseases, Shihezi University School of Medicine, North 4th Road, 832002, Shihezi, China. 39189926@qq.com.
Jin-Fang JiangDepartment of Pathology and Key Laboratory for Xinjiang Endemic and Ethnic Diseases, Shihezi University School of Medicine, North 4th Road, 832002, Shihezi, China. 2106538234@qq.com.
Man LiDepartment of Pathology and Key Laboratory for Xinjiang Endemic and Ethnic Diseases, Shihezi University School of Medicine, North 4th Road, 832002, Shihezi, China. 243083166@qq.com.
Wei-Hua LiangDepartment of Pathology and Key Laboratory for Xinjiang Endemic and Ethnic Diseases, Shihezi University School of Medicine, North 4th Road, 832002, Shihezi, China. 34742913@qq.com.
Yong LiDepartment of CT and MRI, The First Affiliated Hospital, Shihezi University School of Medicine, 832002, Shihezi, China. 24363941@qq.com.
Yu-Tao WeiDepartment of Thoracic and Cardiovascular Surgery, The First Affiliated Hospital, Shihezi University School of Medicine, 832002, Shihezi, China. 53447780@qq.com.
Zhen-Zhu SunDepartment of Pathology, People Hospital of Xinjiang Uygur Autonomous Region, Ürümqi, China. sunzhenzhu@medmail.com.cn.
Chuan-Yue WuDepartment of Pathology and Key Laboratory for Xinjiang Endemic and Ethnic Diseases, Shihezi University School of Medicine, North 4th Road, 832002, Shihezi, China. carywu@pitt.edu.
Yun-Zhao ChenDepartment of Pathology and Key Laboratory for Xinjiang Endemic and Ethnic Diseases, Shihezi University School of Medicine, North 4th Road, 832002, Shihezi, China. cyz0515@sina.com.
Feng LiDepartment of Pathology and Key Laboratory for Xinjiang Endemic and Ethnic Diseases, Shihezi University School of Medicine, North 4th Road, 832002, Shihezi, China. lifeng7855@126.com.
Shihezi University · CNFirst Affiliated Hospital of Shihezi University Medical College · CNPeople's Hospital of Xinjiang Uygur Autonomous Region · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEsophageal squamous cell carcinoma (ESCC) is a highly lethal cancer, and its underlying molecular mechanisms are poorly understood. Recent large-scale genome-wide association studies in Chinese Han populations have identified an ESCC susceptibility locus within the SLC39A6 gene. Here, we sought to explore the expression and biological function of SLC39A6 in ESCC.

methodsMultiethnic validation of SLC39A6 protein expression was performed in different cohorts of patients from Chinese Han and Kazakh populations in the Xinjiang region by immunohistochemistry. The associations among SLC39A6 expression, clinicopathological parameters, and prognosis outcomes of ESCC were analyzed. And the effects of SLC39A6 silencing by siRNA on cell proliferation, apoptosis, and invasiveness, as well as the proteins involved in epithelial-to-mesenchymal transition (EMT) of esophageal cancer cells, were studied.

resultsSLC39A6 protein expression increased progressively from normal esophageal epithelium (NEE) to low-grade intraepithelial neoplasia to ESCC, and finally reached the highest in high-grade intraepithelial neoplasia from Han ethnic. Similarly, SLC39A6 protein was significantly overexpressed in Kazakh ethnic ESCC compared with that in NEE. Increased expression of SLC39A6 was found to be closely correlated with histological grade and early Tumor-Node-Metastasis stage I/II. High tumorous SLC39A6 expression was significantly correlated with shorter overall survival (OS). Cox regression analysis confirmed that SLC39A6 expression was an independent prognostic factor for poor OS in ESCC. Experimentally, the suppression of SLC39A6 expression promoted ESCC cell apoptosis but abrogated proliferation and invasion, and induced an EMT phenotype that included enhanced expression of E-cadherin, loss of vimentin, and morphological changes in ESCC cells in vitro.

conclusionsCombined, our findings highlight a tumor-promoting role for SLC39A6 in ESCC, suggesting that SLC39A6 could serve as an early detector of high-risk subjects and prognostic biomarker. The targeting of SLC39A6 might be a potential therapeutic strategy for blocking ESCC.

Indexed as

AdultAgedAged, 80 and overApoptosisBiomarkers, TumorCarcinomaCation Transport ProteinsCell ProliferationChinaCohort StudiesEpithelial-Mesenchymal TransitionEsophageal NeoplasmsFemaleGenetic Predisposition to DiseaseHumansImmunohistochemistryBiomarkers, TumorCation Transport ProteinsNeoplasm ProteinsRNA, Small InterferingSLC39A6 protein, human

Identifiers

PMID26444413
PMCPMC4595240
OpenAlexW1868978502

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.