Evidence map›Paper›PMID 33579362›Full record

ArticleStem cell research & therapy2021

Alpha-enolase (ENO1), identified as an antigen to monoclonal antibody 12C7, promotes the self-renewal and malignant phenotype of lung cancer stem cells by AMPK/mTOR pathway.

Xiong Shu, Kai-Yue Cao, Hui-Qi Liu, Long Yu, Li-Xin Sun, Zhi-Hua Yang, Cheng-Ai Wu, Yu-Liang Ran

Open access · goldAbstract read
In one paragraph

Article in Stem cell research & therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.0field-weighted citation impact, top 11% 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

20 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
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  7. mFrontiers in cell and developmental biology · 2026
    Review
  8. Article
  9. Article
  10. Role of ENO1 and its targeted therapy in tumors.Journal of translational medicine · 2024
    Review
  11. Article
  12. Article
  13. Article
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  16. Review
  17. Article
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  19. Article
  20. The essential roles of mJournal of experimental & clinical cancer research : CR · 2022
    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

8 authors at 4 institutions in 1 country.

Xiong Shu *Laboratory of Molecular Orthopaedics, Beijing Research Institute of Orthopaedics and Traumatology, Beijing JiShuiTan Hospital, No. 31 Xinjiekou E Road, Xicheng, Beijing, 100035, People's Republic of China.
Kai-Yue Cao *Department of Pathology, Tianjin First Central Hospital, Tianjin, People's Republic of China.
Hui-Qi LiuDepartment of Basic Medical Science, Medical School of Qinghai University, Xining, People's Republic of China.
Long YuState Key Laboratory of Molecular Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, No. 17 Panjiayuan Subdistrict, Chaoyang, Beijing, 100021, People's Republic of China.
Li-Xin SunState Key Laboratory of Molecular Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, No. 17 Panjiayuan Subdistrict, Chaoyang, Beijing, 100021, People's Republic of China.
Zhi-Hua YangState Key Laboratory of Molecular Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, No. 17 Panjiayuan Subdistrict, Chaoyang, Beijing, 100021, People's Republic of China.
Cheng-Ai WuLaboratory of Molecular Orthopaedics, Beijing Research Institute of Orthopaedics and Traumatology, Beijing JiShuiTan Hospital, No. 31 Xinjiekou E Road, Xicheng, Beijing, 100035, People's Republic of China. wuchengai05@163.com.
Yu-Liang RanState Key Laboratory of Molecular Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, No. 17 Panjiayuan Subdistrict, Chaoyang, Beijing, 100021, People's Republic of China. ran_yuliang@126.com.
Chinese Academy of Medical Sciences & Peking Union Medical College · CNPeking University · CNQinghai University · CNTianjin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTumor-associated antigens (TAAs) can be targeted in cancer therapy. We previously identified a monoclonal antibody (mAb) 12C7, which presented anti-tumor activity in lung cancer stem cells (LCSCs). Here, we aimed to identify the target antigen for 12C7 and confirm its role in LCSCs.

methodsImmunofluorescence was used for antigen localization. After targeted antigen purification by electrophoresis and immunoblot, the antigen was identified by LC-MALDI-TOF/TOF mass spectrometry, immunofluorescence, and immunoprecipitation. The overexpression or silence of ENO1 was induced by lentiviral transduction. Self-renewal, growth, and invasion of LCSCs were evaluated by sphere formation, colony formation, and invasion assay, respectively. High-throughput transcriptome sequencing (RNA-seq) and bioinformatics analysis were performed to analyze downstream targets and pathways of targeted antigen.

resultsTargeted antigen showed a surface antigen expression pattern, and the 43-55 kDa protein band was identified as α-enolase (ENO1). Self-renewal, growth, and invasion abilities of LCSCs were remarkably inhibited by ENO1 downregulation, while enhanced by ENO1 upregulation. RNA-seq and bioinformatics analysis eventually screened 4 self-renewal-related and 6 invasion-related differentially expressed genes. GSEA analysis and qRT-PCR verified that ENO1 regulated self-renewal, invasion-related genes, and pathways. KEGG pathway analysis and immunoblot demonstrated that ENO1 inactivated AMPK pathway and activated mTOR pathway in LCSCs.

conclusionsENO1 is identified as a targeted antigen of mAb 12C7 and plays a pivotal role in facilitating self-renewal, growth, and invasion of LCSCs. These findings provide a potent therapeutic target for the stem cell therapy for lung cancer and have potential to improve the anti-tumor activity of 12C7.

Indexed as

NeoplasmsPhosphopyruvate HydrataseAMP-Activated Protein KinasesAntibodies, MonoclonalBiomarkers, TumorCell Line, TumorLungNeoplastic Stem CellsPhenotypeTOR Serine-Threonine KinasesAMP-Activated Protein KinasesAntibodies, MonoclonalBiomarkers, TumorPhosphopyruvate HydrataseTOR Serine-Threonine KinasesCancer stem cellsLung cancerMonoclonal antibodyTumor-associated antigensα-Enolase

Identifiers

PMID33579362
PMCPMC7881626
OpenAlexW3126761174

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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.