Evidence map›Paper›PMID 32489462›Full record

ArticleJournal of Cancer2020

Long non-coding RNA HOTAIR as a competitive endogenous RNA to sponge miR-206 to promote colorectal cancer progression by activating CCL2.

Jia Shengnan, Xie Dafei, Jin Hua, Fan Sunfu, Wang Xiaowei, Xu Liang

Open access · goldAbstract read
In one paragraph

Article in Journal of Cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 2 pooled it
1.5field-weighted citation impact, top 18% 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

23 citing papers in PubMed, 2 syntheses or guidelines pooled it, 29 citations in OpenAlex.

  1. Pooled it
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  10. Exploring the Key Signaling Pathways and ncRNAs in Colorectal Cancer.International journal of molecular sciences · 2024
    Review
  11. Article
  12. HOTAIR in colorectal cancer: structure, function, and therapeutic potential.Medical oncology (Northwood, London, England) · 2023
    Review
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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 1 institution in 1 country.

Jia ShengnanZhejiang Hospital, Hangzhou, 310013, China.
Xie DafeiZhejiang Hospital, Hangzhou, 310013, China.
Jin HuaZhejiang Hospital, Hangzhou, 310013, China.
Fan SunfuZhejiang Hospital, Hangzhou, 310013, China.
Wang XiaoweiZhejiang Hospital, Hangzhou, 310013, China.
Xu LiangZhejiang Hospital, Hangzhou, 310013, China.
Zhejiang Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Colorectal cancer (CRC) is one of the common malignant tumors, the incidence of which is on rise. LncHOTAIR, considered as an oncogene, contributed to the progression of a lot of cancers. However, the molecular mechanism and biological functions of the HOTAIR/miR-206/CCL2 axis have not been reported before. Here, our research aimed to explore HOTAIR/miR-206/CCL2 axis in CRC to demonstrate its role in predicting the poor prognosis of CRC. LncHOTAIR, miR-206 and CCL2 mRNA were detected in CRC tissues and cells by RT-PCR. The interactions among LncHOTAIR, miR-206 and CCL2 were explored by luciferase reporter assay, qRT-PCR, western blot and RNA interfere. Flow Cytometry Cell Analysis was performed to detect cell cycle and apoptosis as well as colony assay was prepared to test the cell proliferation. Immunohistochemical analysis was used to detect the CCL2 protein in CRC tissues. In our study, silence of LncHOTAIR by RNA interference could suppress the proliferation, migration and invasion of CRC cells. Mechanistically, LncHOTAIR downregulated miR-206 abundance which indicated that LncHOTAIR was considered as a competing endogenous RNA (ceRNA) by directly sponging miR-206 in CRC cells. In addition, further exploration suggested that miR-206 could inhibit the function of the downstream CCL2, the expression of which was repressed by LncHOTAIR/miR-206 signaling. Furthermore, we verified that the overexpression of CCL2 attenuated CRC cell proliferation, migration, invasion. Overall, this study firstly elucidated that LncHOTAIR played as oncogene in CRC via directly sponging miR-206 to activate the downstream CCL2, which would be considered as the novel therapeutic target in CRC.

Indexed as

CCL2CRCLong noncoding RNA HOTAIRmircroRNA-206Prognosis

Identifiers

PMID32489462
PMCPMC7255378
OpenAlexW3027730324

What OpenQuestion holds

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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.