Evidence map›Paper›PMID 28939985›Full record

ArticleJournal of molecular medicine (Berlin, Germany)2017

L1CAM drives oncogenicity in esophageal squamous cell carcinoma by stimulation of ezrin transcription.

Jin-Cheng Guo, Yang-Min Xie, Li-Qiang Ran, Hui-Hui Cao, Chun Sun, Jian-Yi Wu, Zhi-Yong Wu, Lian-Di Liao, Wei-Jiang Zhao, Wang-Kai Fang and 4 more

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of molecular medicine (Berlin, Germany), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
4.9field-weighted citation impact, top 4% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Translational cancer research · 2024
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  15. L1CAM as an E-selectin Ligand in Colon Cancer.International journal of molecular sciences · 2020
    Article
  16. Article
  17. Article
  18. Review
  19. Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2019
    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

14 authors at 3 institutions in 1 country.

Jin-Cheng GuoDepartment of Biochemistry and Molecular Biology, Medical College of Shantou University, No. 22 Xinling Road, Shantou, China.
Yang-Min XieDepartment of Experimental Animal Center, Medical College of Shantou University, Shantou, China.
Li-Qiang RanDepartment of Biochemistry and Molecular Biology, Medical College of Shantou University, No. 22 Xinling Road, Shantou, China.
Hui-Hui CaoInstitute of Oncologic Pathology, Medical College of Shantou University, Shantou, China.
Chun SunDepartment of Biochemistry and Molecular Biology, Medical College of Shantou University, No. 22 Xinling Road, Shantou, China.
Jian-Yi WuDepartment of Biochemistry and Molecular Biology, Medical College of Shantou University, No. 22 Xinling Road, Shantou, China.
Zhi-Yong WuDepartment of Oncologic Surgery, Shantou Central Hospital, Affiliated Shantou Hospital of Sun Yat-Sen University, Shantou, China.
Lian-Di LiaoInstitute of Oncologic Pathology, Medical College of Shantou University, Shantou, China.
Wei-Jiang ZhaoCenter for Neuroscience, Medical College of Shantou University, Shantou, China.
Wang-Kai FangDepartment of Biochemistry and Molecular Biology, Medical College of Shantou University, No. 22 Xinling Road, Shantou, China.
En-Min LiDepartment of Biochemistry and Molecular Biology, Medical College of Shantou University, No. 22 Xinling Road, Shantou, China.
Li-Yan XuInstitute of Oncologic Pathology, Medical College of Shantou University, Shantou, China. lyxu@stu.edu.cn.
Melitta SchachnerCenter for Neuroscience, Medical College of Shantou University, Shantou, China. Schachner@dls.rutgers.edu.
Jian-Jun XieDepartment of Biochemistry and Molecular Biology, Medical College of Shantou University, No. 22 Xinling Road, Shantou, China. g_jjxie@stu.edu.cn.
Shantou University · CNShantou University Medical College · CNShantou Central Hospital · CN

Funding

the Fok Ying-Tong Education Foundation No.141034the Natural Science Foundation of China No.81472342; 81172264; 81472613the Natural Science Foundation of China-Guangdong Joint Fund No.U1301227the Science and Technology Program of Guangdong 2013B060300020; 2014A030304060
6 · The paper itself

Abstract

L1 cell adhesion molecule (L1CAM) is highly expressed in various types of human cancers, displaying yet unknown molecular mechanisms underlying their oncogenic potential. Here, we found that L1CAM expression was significantly increased in esophageal squamous cell carcinoma (ESCC; n = 157) lesions compared with non-cancerous tissues. High tumorous L1CAM expression significantly correlated with reduced overall survival. Experimentally, L1CAM knockdown led to decreased cell growth, migration, and invasiveness in vitro, whereas overexpression of L1CAM showed the opposite effect. In nude mice, L1CAM depletion attenuated tumorigenesis and ability to penetrate the tissues surrounding ESCC cells. Gene set enrichment analysis (GSEA) and SubpathwayMiner analysis on gene expression profiles (microarray data on ESCC tissues, GSE53625; cDNA microarray data on L1CAM-knockdown ESCC cell line, GSE86268) suggested that L1CAM-co-expression genes were related to cell motility, cell proliferation, and regulation of actin cytoskeleton, validating the above experimental findings. Further mechanistical analysis showed that L1CAM upregulated the expression of the cytoskeletal protein ezrin via activating integrin β1/MAPK/ERK/AP1 signaling and thus led to the malignant phenotypes of ESCC cells. Together, our findings suggest that L1CAM may be employed as a valuable prognosis marker and a therapeutic target for ESCC patients and that L1CAM promotes ESCC tumorigenicity by upregulating ezrin expression. KEY MESSAGES: L1CAM promotes growth and invasiveness of ESCC cells in vitro and in vivo. L1CAM upregulates the expression of ezrin by integrin α5β1/MAPK/ERK/AP1 pathway. Ezrin is a key downstream effector in the L1CAM-promoted malignant phenotypes. High expression levels of both L1CAM and ezrin significantly correlated with reduced overall survival. Nuclear L1CAM is an independent prognosis marker for esophageal squamous cell carcinoma.

Indexed as

Transcription, GeneticAnimalsBase SequenceCarcinogenesisCarcinoma, Squamous CellCell Line, TumorCell MovementCell ProliferationCell SurvivalCytoskeletal ProteinsEsophageal NeoplasmsEsophageal Squamous Cell CarcinomaEzrinFemaleGene Expression Regulation, NeoplasticGene SilencingCytoskeletal ProteinsEzrinNeural Cell Adhesion Molecule L1Cell malignant phenotypesEsophageal squamous cell carcinomaEzrinL1CAMTranscriptional activation

Identifiers

PMID28939985
OpenAlexW2759355130

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.