Evidence map›Paper›PMID 31287002›Full record

ArticleJournal of experimental & clinical cancer research : CR2019

Long noncoding RNA NEAT1 drives aggressive endometrial cancer progression via miR-361-regulated networks involving STAT3 and tumor microenvironment-related genes.

Peixin Dong, Ying Xiong, Junming Yue, Daozhi Xu, Kei Ihira, Yosuke Konno, Noriko Kobayashi, Yukiharu Todo, Hidemichi Watari

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
101citing papers in PubMed, 1 pooled it
10.2field-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

101 citing papers in PubMed, 1 synthesis or guideline pooled it, 162 citations in OpenAlex.

  1. Pooled it
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  8. Functional, Pharmacogenomic, and Immune Landscapes of Long Non-Coding RNAs in Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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  18. Advances in MiRNAs Involved in Endometrial Carcinoma.Combinatorial chemistry & high throughput screening · 2025
    Review
  19. Article
  20. Article

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

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

9 authors at 5 institutions in 3 countries.

Peixin DongDepartment of Obstetrics and Gynecology, Hokkaido University School of Medicine, Hokkaido University, Sapporo, Japan. dpx1cn@gmail.com.ORCID http://orcid.org/0000-0002-2335-1394
Ying XiongDepartment of Gynecology, State Key Laboratory of Oncology in South China, Sun Yat-sen University Cancer Center, Guangzhou, People's Republic of China.
Junming YueDepartment of Pathology and Laboratory Medicine, University of Tennessee Health Science Center, Memphis, TN, 38163, USA.
Daozhi XuDepartment of Obstetrics and Gynecology, Hokkaido University School of Medicine, Hokkaido University, Sapporo, Japan.
Kei IhiraDepartment of Obstetrics and Gynecology, Hokkaido University School of Medicine, Hokkaido University, Sapporo, Japan.
Yosuke KonnoDepartment of Obstetrics and Gynecology, Hokkaido University School of Medicine, Hokkaido University, Sapporo, Japan.
Noriko KobayashiDepartment of Obstetrics and Gynecology, Hokkaido University School of Medicine, Hokkaido University, Sapporo, Japan.
Yukiharu TodoDivision of Gynecologic Oncology, National Hospital Organization, Hokkaido Cancer Center, Sapporo, Japan.
Hidemichi WatariDepartment of Obstetrics and Gynecology, Hokkaido University School of Medicine, Hokkaido University, Sapporo, Japan. watarih@med.hokudai.ac.jp.
Hokkaido University · JPHokkaido University of Science · JPNational Hospital Organization Hokkaido Medical Center · JPSun Yat-sen University · CNUniversity of Tennessee Health Science Center · US

Funding

Role of MTF1 in ovarian cancerR21CA216585 · NCI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI YUE, JUNMING · 2018 to 2019
$385k
NCI NIH HHS R21 CA216585NIMH NIH HHS 1R21CA216585-01A1
6 · The paper itself

Abstract

backgroundHigh-grade endometrioid and serous endometrial cancers (ECs) are an aggressive subtype of ECs without effective therapies. The reciprocal communication between tumor cells and their surrounding microenvironment drives tumor progression. Long noncoding RNAs (lncRNAs) are key mediators of tumorigenesis and metastasis. However, little is known about the role of lncRNAs in aggressive EC progression and tumor microenvironment remodeling.

methodsWe performed an array-based lncRNA analysis of a parental HEC-50 EC cell population and derivatives with highly invasive, sphere-forming, and paclitaxel (TX)-resistant characteristics. We characterized the roles of the lncRNA NEAT1 in mediating aggressive EC progression in vitro and in vivo and explored the molecular events downstream of NEAT1.

resultsWe identified 10 lncRNAs with upregulated expression (NEAT1, H19, PVT1, UCA1, MIR7-3HG, SNHG16, HULC, RMST, BCAR4 and LINC00152) and 10 lncRNAs with downregulated expression (MEG3, GAS5, DIO3OS, MIR155HG, LINC00261, FENDRR, MIAT, TMEM161B-AS1, HAND2-AS1 and NBR2) in the highly invasive, sphere-forming and TX-resistant derivatives. NEAT1 expression was markedly upregulated in early-stage EC tissue samples, and high NEAT1 expression predicted a poor prognosis. Inhibiting NEAT1 expression with small hairpin RNAs (shRNAs) diminished cellular proliferation, invasion, sphere formation, and xenograft tumor growth and improved TX response in aggressive EC cells. We showed that NEAT1 functions as an oncogenic sponge for the tumor suppressor microRNA-361 (miR-361), which suppresses proliferation, invasion, sphere formation and TX resistance by directly targeting the oncogene STAT3. Furthermore, miR-361 also suppressed the expression of multiple prometastatic genes and tumor microenvironment-related genes, including MEF2D, ROCK1, WNT7A, VEGF-A, PDE4B, and KPNA4.

conclusionsNEAT1 initiates a miR-361-mediated network to drive aggressive EC progression. These data support a rationale for inhibiting NEAT1 signaling as a potential therapeutic strategy for overcoming aggressive EC progression and chemoresistance.

Indexed as

AnimalsCell Line, TumorDisease ProgressionDrug Resistance, NeoplasmEndometrial NeoplasmsFemaleGene Expression Regulation, NeoplasticHeterograftsHumansMiceMice, Inbred BALB CMice, NudeMicroRNAsRNA, Long NoncodingSignal TransductionSTAT3 Transcription FactorMicroRNAsMIRN361 microRNA, humanNEAT1 long non-coding RNA, humanRNA, Long NoncodingSTAT3 protein, humanSTAT3 Transcription FactorEndometrial cancer metastasismiR-361NEAT1STAT3Tumor microenvironment

Identifiers

PMID31287002
PMCPMC6615218
OpenAlexW2959860464

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.