Evidence map›Paper›PMID 35842613›Full record

ArticleMolecular cancer2022

LINE-1 promotes tumorigenicity and exacerbates tumor progression via stimulating metabolism reprogramming in non-small cell lung cancer.

Zeguo Sun, Rui Zhang, Xiao Zhang, Yifei Sun, Pengpeng Liu, Nancy Francoeur, Lei Han, Wan Yee Lam, Zhengzi Yi, Robert Sebra and 3 more

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
4.5field-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

41 citing papers in PubMed, 55 citations in OpenAlex.

  1. Review
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  9. TEITbase: a database for transposable element (TE)-initiated transcripts in human cancers.Database : the journal of biological databases and curation · 2026
    Article
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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

13 authors at 2 institutions in 2 countries.

Zeguo Sun *Department of Medicine, Icahn School of Medicine at Mount Sinai, New York City, NY, USA.
Rui Zhang *Cancer Molecular Diagnostics Core, Tianjin Medical University Cancer Institute & Hospital, National Clinical Research Center of Cancer, Key Laboratory of Cancer Prevention and Therapy, Key Laboratory of Cancer Immunology and Biotherapy, Tianjin's Clinical Research Center for Cancer, Tianjin, China.
Xiao ZhangCancer Molecular Diagnostics Core, Tianjin Medical University Cancer Institute & Hospital, National Clinical Research Center of Cancer, Key Laboratory of Cancer Prevention and Therapy, Key Laboratory of Cancer Immunology and Biotherapy, Tianjin's Clinical Research Center for Cancer, Tianjin, China.
Yifei SunDepartment of Pharmacological Sciences, Icahn School of Medicine at Mount Sinai, New York City, NY, USA.
Pengpeng LiuCancer Molecular Diagnostics Core, Tianjin Medical University Cancer Institute & Hospital, National Clinical Research Center of Cancer, Key Laboratory of Cancer Prevention and Therapy, Key Laboratory of Cancer Immunology and Biotherapy, Tianjin's Clinical Research Center for Cancer, Tianjin, China.
Nancy FrancoeurDepartment of Pharmacological Sciences, Icahn School of Medicine at Mount Sinai, New York City, NY, USA.
Lei HanCancer Molecular Diagnostics Core, Tianjin Medical University Cancer Institute & Hospital, National Clinical Research Center of Cancer, Key Laboratory of Cancer Prevention and Therapy, Key Laboratory of Cancer Immunology and Biotherapy, Tianjin's Clinical Research Center for Cancer, Tianjin, China.
Wan Yee LamDepartment of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York City, NY, USA.
Zhengzi YiDepartment of Medicine, Icahn School of Medicine at Mount Sinai, New York City, NY, USA.
Robert SebraDepartment of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York City, NY, USA.
Martin WalshDepartment of Pharmacological Sciences, Icahn School of Medicine at Mount Sinai, New York City, NY, USA.
Jinpu YuCancer Molecular Diagnostics Core, Tianjin Medical University Cancer Institute & Hospital, National Clinical Research Center of Cancer, Key Laboratory of Cancer Prevention and Therapy, Key Laboratory of Cancer Immunology and Biotherapy, Tianjin's Clinical Research Center for Cancer, Tianjin, China. jyu@tmu.edu.cn.
Weijia ZhangDepartment of Medicine, Icahn School of Medicine at Mount Sinai, New York City, NY, USA. weijia.zhang@mssm.edu.
Icahn School of Medicine at Mount Sinai · USTianjin Medical University Cancer Institute and Hospital · CN

Funding

Underlying chromatin architecture defines functionality for CFTR expressionR01DK118946 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI WALSH, MARTIN JOHN · 2018 to 2022
$2.1M
NIDDK NIH HHS R01 DK118946
6 · The paper itself

Abstract

backgroundLong Interspersed Nuclear Element-1 (LINE-1, L1) is increasingly regarded as a genetic risk for lung cancer. Transcriptionally active LINE-1 forms a L1-gene chimeric transcript (LCTs), through somatic L1 retrotransposition (LRT) or L1 antisense promoter (L1-ASP) activation, to play an oncogenic role in cancer progression.

methodsHere, we developed Retrotransposon-gene fusion estimation program (ReFuse), to identify and quantify LCTs in RNA sequencing data from TCGA lung cancer cohort (n = 1146) and a single cell RNA sequencing dataset then further validated those LCTs in an independent cohort (n = 134). We next examined the functional roles of a cancer specific LCT (L1-FGGY) in cell proliferation and tumor progression in LUSC cell lines and mice.

resultsThe LCT events correspond with specific metabolic processes and mitochondrial functions and was associated with genomic instability, hypomethylation, tumor stage and tumor immune microenvironment (TIME). Functional analysis of a tumor specific and frequent LCT involving FGGY (L1-FGGY) reveal that the arachidonic acid (AA) metabolic pathway was activated by the loss of FGGY through the L1-FGGY chimeric transcript to promote tumor growth, which was effectively targeted by a combined use of an anti-HIV drug (NVR) and a metabolic inhibitor (ML355). Lastly, we identified a set of transcriptomic signatures to stratify the LUSC patients with a higher risk for poor outcomes who may benefit from treatments using NVR alone or combined with an anti-metabolism drug.

conclusionsThis study is the first to characterize the role of L1 in metabolic reprogramming of lung cancer and provide rationale for L1-specifc prognosis and potential for a therapeutic strategy for treating lung cancer.

trial registrationStudy on the mechanisms of the mobile element L1-FGGY promoting the proliferation, invasion and immune escape of lung squamous cell carcinoma through the 12-LOX/Wnt pathway, Ek2020111. Registered 27 March 2020 - Retrospectively registered.

Indexed as

Carcinoma, Non-Small-Cell LungCarcinoma, Squamous CellLung NeoplasmsAnimalsCell Line, TumorGene Expression Regulation, NeoplasticHumansMicePrognosisTumor MicroenvironmentFGGYLINE-1LUADLUSCMetabolicNSCLCTransposable element

Identifiers

PMID35842613
PMCPMC9288060
OpenAlexW4285588679

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.