Evidence map›Paper›PMID 32694942›Full record

ArticleCancer cell international2020

Long noncoding RNA HOTAIR promotes breast cancer development by targeting ZEB1 via sponging miR-601.

Yuanyuan Wang, Guoliang Gong, Jingyun Xu, Yuanxin Zhang, Shenggui Wu, Shaohong Wang

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer cell international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 13% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

  1. Pooled it
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  9. The Role of M6A LncRNA Modification in Papillary Thyroid Cancer.International journal of molecular sciences · 2025
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  12. Long noncoding RNA HOTAIR promotes breast cancer development through the lncRNA HOTAIR/miR-1/GOLPH3 axis.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
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  17. Roles and Mechanisms of Long Non-Coding RNAs in Breast Cancer.International journal of molecular sciences · 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

6 authors at 2 institutions in 1 country.

Yuanyuan WangDepartment of Pathology, Shantou Central Hospital and Affiliated Shantou Hospital of Sun Yat-Sen University, Shantou, 515000 China.
Guoliang GongDepartment of Pathology, The First Affiliated Hospital of Shantou University Medical College, No. 57, Changping Road, Shantou, 515041 Guangdong China.ORCID 0000-0002-5636-7069
Jingyun XuDepartment of Pathology, The First Affiliated Hospital of Shantou University Medical College, No. 57, Changping Road, Shantou, 515041 Guangdong China.
Yuanxin ZhangDepartment of Pathology, Chaonan Minsheng Hospital of Shantou, Shantou, 515000 China.
Shenggui WuDepartment of Pathology, Chaonan Minsheng Hospital of Shantou, Shantou, 515000 China.
Shaohong WangDepartment of Pathology, Shantou Central Hospital and Affiliated Shantou Hospital of Sun Yat-Sen University, Shantou, 515000 China.
Shantou Central Hospital · CNShantou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBreast cancer (BC) is a common malignancy worldwide. It has been reported that long non-coding RNA (lncRNA) HOX transcript antisense RNA (HOTAIR) is abnormally expressed in BC. However, the role of HOTAIR in the malignancy of BC is worth further discussion. This study aims to clarify the function and molecular mechanism of HOTAIR in BC.

methodsQuantitative real-time polymerase chain reaction (qRT-PCR) was employed to determine the expression of HOTAIR, microRNA (miR)-601 and zinc finger E-box binding homeobox 1 (ZEB1). Cell counting kit-8 (CCK-8) and transwell assay were used to detect the proliferation, migration and invasion of cells. Further, the protein levels of AKT, phosphorylated-AKT (p-AKT), ZEB1 and Ki-67 were confirmed by western blot (WB) assay. Moreover, dual-luciferase reporter assay was applied to examine the targeting relationship between HOTAIR and miR-601 or miR-601 and ZEB1. In addition, animal experiments were conducted to verify the effect of HOTAIR on BC tumor growth in vivo.

resultsHOTAIR was upregulated in BC tissues and cells, and its knockdown suppressed the proliferation, migration, invasion and the activity of AKT signaling pathway of BC cells. HOTAIR could serve as a sponge of miR-601. Further experiments revealed that miR-601 inhibitor could reverse the inhibition effect of HOTAIR silencing on the progression of BC. Meanwhile, ZEB1 was a target of miR-601, and its overexpression could invert the suppression effect of miR-601 overexpression on the progression of BC. Additionally, ZEB1 expression was regulated by HOTAIR and miR-601. Furthermore, interference of HOTAIR could attenuate BC tumor growth in vivo.

conclusionIn short, this study demonstrated that HOTAIR promoted the proliferation, migration, invasion of BC through regulating the miR-601/ZEB1 axis, which provided a theoretical basis for the research on lncRNA-directed therapeutics in BC.

Indexed as

AKT signaling pathwayBCHOTAIRmiR-601ZEB1

Identifiers

PMID32694942
PMCPMC7367248
OpenAlexW3042423832

What OpenQuestion holds

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LicenceCC BY
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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.