Evidence map›Paper›PMID 30787392›Full record

ArticleCell death and differentiation2019

Long noncoding RNA LINC00336 inhibits ferroptosis in lung cancer by functioning as a competing endogenous RNA.

Min Wang, Chao Mao, Lianlian Ouyang, Yating Liu, Weiwei Lai, Na Liu, Ying Shi, Ling Chen, Desheng Xiao, Fenglei Yu and 7 more

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in Cell death and differentiation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 346 papers.

0numbers the graph read from it
0cells of the map it votes in
346citing papers in PubMed
29.3field-weighted citation impact, top 1% 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

346 citing papers in PubMed, 580 citations in OpenAlex.

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286 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors at 3 institutions in 3 countries.

Min WangKey Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Department of Pathology, Xiangya Hospital, Central South University, Changsha, Hunan, 410078, China.
Chao MaoKey Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Department of Pathology, Xiangya Hospital, Central South University, Changsha, Hunan, 410078, China.
Lianlian OuyangKey Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Department of Pathology, Xiangya Hospital, Central South University, Changsha, Hunan, 410078, China.
Yating LiuKey Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Department of Pathology, Xiangya Hospital, Central South University, Changsha, Hunan, 410078, China.
Weiwei LaiKey Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Department of Pathology, Xiangya Hospital, Central South University, Changsha, Hunan, 410078, China.
Na LiuKey Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Department of Pathology, Xiangya Hospital, Central South University, Changsha, Hunan, 410078, China.
Ying ShiKey Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Department of Pathology, Xiangya Hospital, Central South University, Changsha, Hunan, 410078, China.
Ling ChenKey Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Department of Pathology, Xiangya Hospital, Central South University, Changsha, Hunan, 410078, China.
Desheng XiaoDepartment of Pathology, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China.
Fenglei YuDepartment of Thoracic Surgery, Second Xiangya Hospital, Central South University, Changsha, 410011, China.
Xiang WangDepartment of Thoracic Surgery, Second Xiangya Hospital, Central South University, Changsha, 410011, China.
Hu ZhouShanghai Institute of Material Medica, Chinese Academy of Sciences (CAS), 555 Zu Chongzhi Road, Zhangjiang Hi-Tech Park, Shanghai, 201203, China.
Ya CaoKey Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Department of Pathology, Xiangya Hospital, Central South University, Changsha, Hunan, 410078, China.
Shuang LiuDepartment of Oncology, Institute of Medical Sciences, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China.
Qin YanDepartment of Pathology, Yale School of Medicine, New Haven, CT, 06520, USA.ORCID http://orcid.org/0000-0003-4077-453X
Yongguang TaoKey Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Department of Pathology, Xiangya Hospital, Central South University, Changsha, Hunan, 410078, China. taoyong@csu.edu.cn.ORCID http://orcid.org/0000-0003-2354-5321
Bin ZhangDepartment of Histology and Embryology, School of Basic Medicine, Central South University, Changsha, Hunan, 410013, China. coolzhangbin22@163.com.
Central South University · CNChinese Academy of Sciences · CNYale University · US

Funding

Yale Clinical and Translational Science Award (U Component)UL1TR001863 · NCATS · YALE UNIVERSITY · PI John H. Krystal, LUCILA OHNO-MACHADO · 2016 to 2026
$102.9M
NCATS NIH HHS UL1 TR001863
6 · The paper itself

Abstract

The regulatory loop between long noncoding RNAs (lncRNAs) and microRNAs has a dynamic role in transcriptional and translational regulation, and is involved in cancer. However, the regulatory circuitry between lncRNAs and microRNAs in tumorigenesis remains elusive. Here we demonstrate that a nuclear lncRNA LINC00336 is upregulated in lung cancer and functions as an oncogene by acting as a competing endogenous RNA (ceRNAs). LINC00336 bound RNA-binding protein ELAVL1 (ELAV-like RNA-binding protein 1) using nucleotides 1901-2107 of LINC00336 and the RRM interaction domain and key amino acids (aa) of ELAVL1 (aa 101-213), inhibiting ferroptosis. Moreover, ELAVL1 increased LINC00336 expression by stabilizing its posttranscriptional level, whereas LSH (lymphoid-specific helicase) increased ELAVL1 expression through the p53 signaling pathway, further supporting the hypothesis that LSH promotes LINC00336 expression. Interestingly, LINC00336 served as an endogenous sponge of microRNA 6852 (MIR6852) to regulate the expression of cystathionine-β-synthase (CBS), a surrogate marker of ferroptosis. Finally, we found that MIR6852 inhibited cell growth by promoting ferroptosis. These data show that the network of lncRNA and ceRNA has an important role in tumorigenesis and ferroptosis.

Indexed as

A549 CellsAnimalsCell Line, TumorCell ProliferationCell SurvivalCystathionine beta-SynthaseELAV-Like Protein 1FerroptosisGene Expression Regulation, NeoplasticGene Regulatory NetworksHumansLung NeoplasmsMiceMice, NudeMicroRNAsNeoplasm TransplantationCystathionine beta-SynthaseELAVL1 protein, humanELAV-Like Protein 1MicroRNAsRNA, Long NoncodingRNA, MessengerTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID30787392
PMCPMC6889193
OpenAlexW2916543168

What OpenQuestion holds

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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.