Evidence map›Paper›PMID 31841994›Full record

ArticleMolecular therapy. Nucleic acids2020

Long Noncoding RNA LINC01116 Contributes to Gefitinib Resistance in Non-small Cell Lung Cancer through Regulating IFI44.

He Wang, Binbin Lu, Shengnan Ren, Fubin Wu, Xinxing Wang, Caiyun Yan, Zhaoxia Wang

Open access · goldAbstract read
In one paragraph

Article in Molecular therapy. Nucleic acids, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed, 1 pooled it
4.4field-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

60 citing papers in PubMed, 1 synthesis or guideline pooled it, 81 citations in OpenAlex.

  1. Pooled it
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  9. LncRNANon-coding RNA research · 2025
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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

7 authors at 2 institutions in 1 country.

He WangDepartment of Oncology, The Second Affiliated Hospital of Nanjing Medical University, Nanjing 210011, People's Republic of China; Department of Oncology, Sir Run Run Hospital, Nanjing Medical University, Nanjing 211166, People's Republic of China.
Binbin LuDepartment of Oncology, The Second Affiliated Hospital of Nanjing Medical University, Nanjing 210011, People's Republic of China.
Shengnan RenDepartment of Oncology, The Second Affiliated Hospital of Nanjing Medical University, Nanjing 210011, People's Republic of China; Department of Oncology, Sir Run Run Hospital, Nanjing Medical University, Nanjing 211166, People's Republic of China.
Fubin WuDepartment of Oncology, Sir Run Run Hospital, Nanjing Medical University, Nanjing 211166, People's Republic of China.
Xinxing WangDepartment of Oncology, Sir Run Run Hospital, Nanjing Medical University, Nanjing 211166, People's Republic of China.
Caiyun YanDepartment of Oncology, Sir Run Run Hospital, Nanjing Medical University, Nanjing 211166, People's Republic of China.
Zhaoxia WangDepartment of Oncology, The Second Affiliated Hospital of Nanjing Medical University, Nanjing 210011, People's Republic of China; Cancer Medical Center, The Second Affiliated Hospital of Nanjing Medical University, Nanjing 210011, People's Republic of China. Electronic address: zhaoxiawang66@126.com.
Nanjing Medical University · CNSecond Affiliated Hospital of Nanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs), such as gefitinib, have been established as first-line treatments for non-small cell lung cancer (NSCLC) patients and have exhibited notable clinical efficacy. However, resistance to TKIs has become one of the major obstacles in improving the therapeutic efficacy of patients with NSCLC. This study aims to investigate the role of the long non-coding RNA (lncRNA) LINC01116 in gefitinib resistance of NSCLC and explore its underlying mechanism. In this study, we found that LINC01116 is upregulated in the gefitinib-resistant NSCLC cells and tissues. Loss- and gain-of-function assays uncovered that LINC01116 downregulation sensitized gefitinib resistance, whereas the overexpression of LINC01116 conferred PC9/R cells to gefitinib resistance. Moreover, LINC01116 silencing increased IFI44 expression. Overexpression of IFI44 reversed the resistance to gefitinib in PC9/R cells, and rescue experiments confirmed that LINC01116 affects the gefitinib resistance of PC9/R cells partly dependent on regulating IFI44 expression. Moreover, downregulation of LINC01116 increased the sensitivity of PC9/R cells to gefitinib in vivo. Our study demonstrates that LINC01116 plays a critical role in gefitinib resistance of NSCLC cells by affecting IFI44 expression, providing a novel therapeutic target to overcome TKI resistance in NSCLC.

Indexed as

gefitinibIFI44LINC01116NSCLCTKI resistance

Identifiers

PMID31841994
PMCPMC6920314
OpenAlexW2983686642

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.