Evidence map›Paper›PMID 36820953›Full record

ArticleClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2023

ENO1 promotes immunosuppression and tumor growth in pancreatic cancer.

Chen Kai Huang, Lei Lv, Huanliang Chen, Ying Sun, Yong Ping

Abstract read
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In one paragraph

Article in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–field-weighted citation impact
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

11 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Role of ENO1 and its targeted therapy in tumors.Journal of translational medicine · 2024
    Review
  9. Article
  10. Article
  11. 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

5 authors.

Chen Kai HuangDepartment of Molecular and Cellular Biology, University of California, Berkeley, 110 Sproul Hall, Berkeley, CA, 94720, USA.
Lei LvMOE Key Laboratory of Metabolism and Molecular Medicine, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fudan University, Shanghai, 200032, China.
Huanliang ChenDepartment of Oncology, Shanghai General Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 201620, China.
Ying SunDepartment of Immunology and Microbiology, School of Medicine, Shanghai Jiao Tong University, 280 South Chongqing Road, Shanghai, 200025, China. sunyingying@sjtu.edu.cn.
Yong PingBio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders (Ministry of Education), Shanghai Jiao Tong University, Shanghai, 200240, China. yoping@sjtu.edu.cn.ORCID http://orcid.org/0000-0003-1066-5471

Funding

Science and Technology Innovation Plan Of Shanghai Science and Technology Commission 18ZR1419400Shanghai Jiao Tong University Foundation YG2022QN033Shanghai Rising-Star Program 19QA1404900
6 · The paper itself

Abstract

backgroundPancreatic adenocarcinoma (PAAD) is a highly aggressive and malignant cancer type with the highest mortality rate of all major cancers. However, the molecular and tumor immune escape mechanism underlying pancreatic cancer remains largely unclear. α-enolase (ENO1) is a glycolytic enzyme reported to overexpress in a variety of cancer types. This study was undertaken to investigate the functional role and therapeutic potential of ENO1 in pancreatic cancer.

methodsWe examined the expression levels of ENO1 across a broad spectrum of cancer types from the TCGA database. ENO1-knockout (ENO1-KO) through CRISPR/CAS9 technology in a mouse pancreatic cancer cell line (PAN02) was used to analyze the role of ENO1 on proliferation and colony formation. Flow cytometry and RT-PCR were also applied to analyze T lymphocytes and relevant cytokines.

resultsIn the present study, we identified that ENO1 promoted pancreatic cancer cell proliferation. Our bioinformatics data indicated that ENO1 was significantly overexpressed in pancreatic cancer cell lines and tissues. Survival analyses revealed that ENO1 overexpression implicated poor survival of PAAD patients. Knockout of ENO1 expression repressed the ability of proliferation and colony formation in PAN02. In addition, ENO1-KO significantly decreased tumor growth in mouse models. Further flow cytometry and RT-PCR analysis revealed that ENO1-KO modulates the tumor microenvironment (TME), especially in suppressed Treg cells and inducing anti-tumor cytokine responses.

conclusionsTaken together, our data showed that ENO1 was an oncogenic biomarker and might serve as a promising target for immunotherapy of pancreatic cancer.

Indexed as

AdenocarcinomaPancreatic NeoplasmsAnimalsBiomarkers, TumorCell Line, TumorImmunosuppression TherapyMiceMice, KnockoutPhosphopyruvate HydrataseTumor MicroenvironmentBiomarkers, TumorEno1 protein, mousePhosphopyruvate HydrataseCytokineENO1Knockout/CrisprPancreatic cancerTregTumor immunology

Identifiers

PMID36820953

What OpenQuestion holds

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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.