Evidence map›Paper›PMID 30545354›Full record

ArticleMolecular cancer2018

LncHOXA10 drives liver TICs self-renewal and tumorigenesis via HOXA10 transcription activation.

Ming Shao, Qiankun Yang, Weitao Zhu, Huifang Jin, Jing Wang, Jie Song, Yongkui Kong, Xianping Lv

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.6field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

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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

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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

36 citing papers in PubMed, 48 citations in OpenAlex.

  1. Review
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  8. Translational cancer research · 2023
    Article
  9. Retraction Note: LncMAPK6 drives MAPK6 expressionand liver TIC self-renewal.Journal of experimental & clinical cancer research : CR · 2022
    Article
  10. Article
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  13. The emerging role of ISWI chromatin remodeling complexes in cancer.Journal of experimental & clinical cancer research : CR · 2021
    Review
  14. Article
  15. Article
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  19. Alternative splicing of lncRNAs in human diseases.American journal of cancer research · 2021
    Review
  20. Article
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

8 authors at 1 institution in 1 country.

Ming ShaoDepartment of Blood Transfusion, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, Henan Province, China.
Qiankun YangDepartment of Blood Transfusion, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, Henan Province, China.
Weitao ZhuDepartment of Clinical Laboratory, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, Henan Province, China.
Huifang JinDepartment of Blood Transfusion, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, Henan Province, China.
Jing WangDepartment of Blood Transfusion, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, Henan Province, China.
Jie SongDepartment of Blood Transfusion, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, Henan Province, China.
Yongkui KongDepartment of Blood Transfusion, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, Henan Province, China.
Xianping LvDepartment of Blood Transfusion, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, Henan Province, China. 848663760@qq.com.
First Affiliated Hospital of Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLiver cancer is one of the most deadly cancers in the world. There are various cells in liver tumor bulk, including liver tumor initiating cells (TICs), which account for liver tumorigenesis, drug resistance, relapse and metastasis. The homeobox (HOX) transcription factors play critical roles in many physiological and pathological processes, while, their roles in liver TICs and liver tumorigenesis remain unknown.

methodsAn unbiased screening was performed using online-available datasets. Liver TICs were sorted by FACS using surface markers CD133, CD13 and EPCAM, or enriched by oncosphere formation assay. TIC self-renewal was examined by oncosphere formation and tumor initiation assay. Loss of function and gain of function assays were performed to examine the role of lncRNA. RNA pulldown, RNA immunoprecipitation, ChIP, Western blot and double FISH were used to explore the molecular mechanism of lncRNA.

resultsHere, we examined the expression pattern of HOX transcription factors, and found HOXA10 was overexpressed in liver cancer samples. Moreover, a divergent lncRNA of HOXA10 (termed lncHOXA10 hereafter) was also highly expressed in liver cancer and liver TICs. LncHOXA10 drove liver TIC self-renewal and liver tumorigenesis through HOXA10-dependent manner. LncHOXA10 interacted with SNF2L and recruited NURF chromatin remodeling complex to HOXA10 promoter, and thus initiated the transcription of HOXA10. Through HOXA10 transcriptional regulation, lncHOXA10 activated HOXA10 in liver TICs. LncHOXA10-HOXA10 signaling can be targeted to eliminate liver TICs. Altogether, lncHOXA10 drove HOXA10 expression and thus promoted liver TIC self-renewal.

conclusionHOXA10 was the most highly expressed HOX transcription factor in liver cancer and liver TICs. LncHOXA10 drove the transcriptional activation of HOXA10. This work revealed the important role of HOX transcription factor in liver TIC self-renewal and added a new layer for liver TIC regulation.

Indexed as

AgedAnimalsCarcinogenesisCarcinoma, HepatocellularCell LineCell Line, TumorDNA-Binding ProteinsFemaleHEK293 CellsHomeobox A10 ProteinsHomeodomain ProteinsHumansLiver NeoplasmsMaleMiceMice, Inbred BALB CDNA-Binding ProteinsHomeobox A10 ProteinsHomeodomain ProteinsHOXA10 protein, humanRNA, Long NoncodingHOX transcription factorLiver cancerLong noncoding RNATumor initiating cells

Identifiers

PMID30545354
PMCPMC6293550
OpenAlexW2904508384

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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.