Evidence map›Paper›PMID 28918035›Full record

ArticleMolecular therapy. Nucleic acids2017

lncRNA HOTAIR Contributes to 5FU Resistance through Suppressing miR-218 and Activating NF-κB/TS Signaling in Colorectal Cancer.

Peilong Li, Xin Zhang, Lili Wang, Lutao Du, Yongmei Yang, Tong Liu, Chen Li, Chuanxin Wang

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

Article in Molecular therapy. Nucleic acids, 2017. 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 82 papers.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed
5.6field-weighted citation impact, top 3% 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

82 citing papers in PubMed, 137 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. LncRNA-Histone Modification Crosstalk: Orchestrating Cancer Pathobiology.Naunyn-Schmiedeberg's archives of pharmacology · 2025
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  6. Review
  7. Review
  8. Role ofMolecular biology research communications · 2025
    Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Expression ofMolecular therapy. Nucleic acids · 2023
    Article
  17. Crosstalk between long noncoding RNA and microRNA in Cancer.Cellular oncology (Dordrecht, Netherlands) · 2023
    Review
  18. Article
  19. Article
  20. Review

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Peilong LiDepartment of Clinical Laboratory, The Second Hospital of Shandong University, Jinan, 250033 Shandong Province, China.
Xin ZhangDepartment of Clinical Laboratory, Qilu Hospital, Shandong University, Jinan, 250012 Shandong Province, China.
Lili WangDepartment of Clinical Laboratory, Qilu Hospital, Shandong University, Jinan, 250012 Shandong Province, China.
Lutao DuDepartment of Clinical Laboratory, Qilu Hospital, Shandong University, Jinan, 250012 Shandong Province, China.
Yongmei YangDepartment of Clinical Laboratory, Qilu Hospital, Shandong University, Jinan, 250012 Shandong Province, China.
Tong LiuDepartment of Clinical Laboratory, The Second Hospital of Shandong University, Jinan, 250033 Shandong Province, China.
Chen LiDepartment of Clinical Laboratory, The Second Hospital of Shandong University, Jinan, 250033 Shandong Province, China.
Chuanxin WangDepartment of Clinical Laboratory, The Second Hospital of Shandong University, Jinan, 250033 Shandong Province, China. Electronic address: cxwang@sdu.edu.cn.
Qilu Hospital of Shandong University · CNSecond Hospital of Shandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

One major reason for the failure of advanced colorectal cancer (CRC) treatment is the occurrence of chemoresistance to fluoropyrimidine (FU)-based chemotherapy. Long non-coding RNA HOTAIR has been considered as a pro-oncogene in multiple cancers. However, the precise functional mechanism of HOTAIR in chemoresistance is not well known. In this study, we investigated the biological and clinical role of HOTAIR in 5FU resistance in CRC. Our results showed that HOTAIR negatively regulated miR-218 expression in CRC through an EZH2-targeting miR-218-2 promoter regulatory axis. HOTAIR knockdown dramatically inhibited cell viability and induced G1-phase arrest by promoting miR-218 expression. VOPP1 was shown to be a functional target of miR-218, and the main downstream signaling, NF-κB, was inactivated by HOTAIR through the suppression of miR-218 expression. Additionally, HOTAIR knockdown partially reversed 5FU resistance through promoting miR-218 and inactivating NF-κB signaling. Furthermore, HOTAIR restrained 5FU-induced cytotoxicity on CRC cells through promotion of thymidylate synthase expression. More importantly, high HOTAIR expression was associated with poor response to 5FU treatment. In conclusion, we demonstrated that HOTAIR contributes to 5FU resistance through suppressing miR-218 and activating NF-κB signaling in CRC. Thus, HOTAIR may serve as a promising therapeutic target for CRC patients.

Indexed as

5-fluorouracilcolorectal cancerHOTAIRmiR-218NF-κBthymidylate synthase

Identifiers

PMID28918035
PMCPMC5537205
OpenAlexW2724290755

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.