Evidence map›Paper›PMID 33446634›Full record

ArticleCell death & disease2021

LncRNA TINCR favors tumorigenesis via STAT3-TINCR-EGFR-feedback loop by recruiting DNMT1 and acting as a competing endogenous RNA in human breast cancer.

Qin Wang, Jiena Liu, Zilong You, Yanling Yin, Lei Liu, Yujuan Kang, Siwei Li, Shipeng Ning, Hui Li, Yajie Gong and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 6% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

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  18. LncRNA-mediated DNA methylation: an emerging mechanism in cancer and beyond.Journal of experimental & clinical cancer research : CR · 2022
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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

12 authors at 1 institution in 1 country.

Qin WangDepartment of Breast Surgery, Harbin Medical University Cancer Hospital, Harbin, China.
Jiena LiuDepartment of Breast Surgery, Harbin Medical University Cancer Hospital, Harbin, China.
Zilong YouDepartment of Breast Surgery, Harbin Medical University Cancer Hospital, Harbin, China.
Yanling YinDepartment of Breast Surgery, Harbin Medical University Cancer Hospital, Harbin, China.
Lei LiuDepartment of Breast Surgery, Harbin Medical University Cancer Hospital, Harbin, China.
Yujuan KangDepartment of Breast Surgery, Harbin Medical University Cancer Hospital, Harbin, China.
Siwei LiDepartment of Breast Surgery, Harbin Medical University Cancer Hospital, Harbin, China.
Shipeng NingDepartment of Breast Surgery, Harbin Medical University Cancer Hospital, Harbin, China.
Hui LiDepartment of Breast Surgery, Harbin Medical University Cancer Hospital, Harbin, China.
Yajie GongDepartment of Breast Surgery, Harbin Medical University Cancer Hospital, Harbin, China.
Shouping XuDepartment of Breast Surgery, Harbin Medical University Cancer Hospital, Harbin, China. Shoupingxu@hrbmu.edu.cn.
Da PangDepartment of Breast Surgery, Harbin Medical University Cancer Hospital, Harbin, China. pangda@ems.hrbmu.edu.cn.ORCID 0000-0003-2853-4170
Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The long noncoding RNA (lncRNA) TINCR has recently been found to be associated with the progression of human malignancies, but the molecular mechanism of TINCR action remains elusive, particularly in breast cancer. The oncogenic role of TINCR was examined in vitro and in vivo in breast cancer. Next, the interaction between TINCR, DNMT1, and miR-503-5p methylation was explored. Moreover, the mechanism by which TINCR enhances EGFR expression and downstream signaling via an RNA-RNA interaction was comprehensively investigated. Furthermore, upstream transcriptional regulation of TINCR expression by STAT3 was examined by performing chromatin immunoprecipitation. Finally, feedback signaling in the STAT3-TINCR-EGFR downstream cascade was also investigated. TINCR is upregulated in human breast cancer tissues, and TINCR knockdown suppresses tumorigenesis in vitro and in vivo. Mechanistically, TINCR recruits DNMT1 to the miR-503-5p locus promoter, which increases the methylation and suppresses the transcriptional expression of miR-503-5p. Furthermore, TINCR also functions as a competing endogenous RNA to upregulate EGFR expression by sponging miR-503-5p. In addition, TINCR stimulates JAK2-STAT3 signaling downstream from EGFR, and STAT3 reciprocally enhances the transcriptional expression of TINCR. Our findings broaden the current understanding of the diverse manners in which TINCR functions in cancer biology. The newly identified STAT3-TINCR-EGFR-feedback loop could serve as a potential therapeutic target for human cancer.

Indexed as

Breast NeoplasmsCarcinogenesisCell Line, TumorCell ProliferationDNA (Cytosine-5-)-Methyltransferase 1ErbB ReceptorsFemaleHumansRNA, Long NoncodingRNA, NeoplasmSTAT3 Transcription FactorDNA (Cytosine-5-)-Methyltransferase 1DNMT1 protein, humanEGFR protein, humanErbB ReceptorsRNA, Long NoncodingRNA, NeoplasmSTAT3 protein, humanSTAT3 Transcription FactorTINCR lncRNA, human

Identifiers

PMID33446634
PMCPMC7809450
OpenAlexW3119920749

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.