Evidence map›Paper›PMID 34627260›Full record

ArticleCancer cell international2021

AL355338 acts as an oncogenic lncRNA by interacting with protein ENO1 to regulate EGFR/AKT pathway in NSCLC.

Qian Hua, Dongliang Wang, Lin Zhao, Zhihui Hong, Kairu Ni, Yizhen Shi, Zengli Liu, Baoming Mi

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

16 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Role of ENO1 and its targeted therapy in tumors.Journal of translational medicine · 2024
    Review
  6. Article
  7. Article
  8. RNA-binding proteinJournal of gastrointestinal oncology · 2023
    Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Review
  16. 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 2 institutions in 1 country.

Qian Hua *Department of Nuclear Medicine, The Second Affiliated Hospital of Soochow University, Suzhou, 215004, Jiangsu, China.
Dongliang Wang *Department of Nuclear Medicine, Fudan University Shanghai Cancer Center, Fudan University, Shanghai, 200032, China.
Lin Zhao *State Key Laboratory of Radiation Medicine and Protection, School of Radiation Medicine and Protection, Collaborative Innovation Center of Radiation Medicine of Jiangsu Higher Education Institutions, Soochow University, Suzhou, China.
Zhihui HongDepartment of Nuclear Medicine, The Second Affiliated Hospital of Soochow University, Suzhou, 215004, Jiangsu, China.
Kairu NiDepartment of Nuclear Medicine, The Second Affiliated Hospital of Soochow University, Suzhou, 215004, Jiangsu, China.
Yizhen ShiDepartment of Nuclear Medicine, The Second Affiliated Hospital of Soochow University, Suzhou, 215004, Jiangsu, China.
Zengli LiuDepartment of Nuclear Medicine, The Second Affiliated Hospital of Soochow University, Suzhou, 215004, Jiangsu, China. liuzengli@126.com.
Baoming MiDepartment of Nuclear Medicine, The Second Affiliated Hospital of Soochow University, Suzhou, 215004, Jiangsu, China. mibaoming@suda.edu.cn.ORCID http://orcid.org/0000-0003-2274-8776
Soochow University · CNFudan University Shanghai Cancer Center · CN

Funding

doctoral research funding project of the Second Affiliated Hospital of Soochow University SDFEYBS2012doctoral research funding project of the Second Affiliated Hospital of Soochow University SDFEYBS2013Jiangsu Postdoctoral Research Foundation 1601121CNational Natural Science Foundation of China 81703159National Natural Science Foundation of China 82073482Natural Science Foundation of Jiangsu Province 81830052Natural Science Foundation of Jiangsu Province BK20210088Suzhou Municipal Science and Technology Bureau KJXW2020016the research funding project of the Second Affiliated Hospital of Soochow University XKTJ-HRC2021003
6 · The paper itself

Abstract

backgroundNon-small cell lung cancer (NSCLC) is a malignancy with considerable morbidity and mortality. Abnormal metabolism is a hallmark of cancer; however, the mechanism of glycolysis regulation in NSCLC progression is not completely understood. Recent studies suggest that some dysregulated long non-coding RNAs (lncRNAs) play important roles in tumor metabolic reprogramming.

methodsTo identify glycolysis-associated-lncRNAs in NSCLC, we compared RNA-sequencing results between high

resultsAL355338 was an upregulated glycolysis-associated lncRNA in NSCLC. Functional assays revealed that AL355338 was critical for promoting aerobic glycolysis and NSCLC progression. Mechanistic investigations showed that AL355338 directly bound with alpha-enolase (ENO1) and enhanced the protein's stability by modulating its degradation and ubiquitination. A positive correlation was observed between AL355338 and ENO1 in NSCLC, and ENO1 was subsequently confirmed to be responsible for the oncogenic role of AL355338. Furthermore, AL355338 was capable of modulating ENO1/EGFR complex interaction and further activating EGFR-AKT signaling.

conclusionsThis study indicates that AL355338 confers an aggressive phenotype to NSCLC, and targeting it might be an effective therapeutic strategy.

Indexed as

Aerobic glycolysisAL355338EGFRENO1Long noncoding RNAs

Identifiers

PMID34627260
PMCPMC8502354
OpenAlexW3194993816

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.