Evidence map›Paper›PMID 34079750›Full record

ArticleFrontiers in oncology2020

CXCL1 Regulated by miR-302e Is Involved in Cell Viability and Motility of Colorectal Cancer

Biyin Chen, Li Song, Xiuzhen Nie, Fangfeng Lin, Zongyang Yu, Wencui Kong, Xiaoyan Qi, Wenwu Wang

Open access · goldAbstract read
In one paragraph

Article in Frontiers in oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.5field-weighted citation impact, top 8% 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

31 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
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  3. Transcriptome sequencing (RNA-Seq) reveals non-coding pseudogene CDC27P9 role in cervical cancer.Apoptosis : an international journal on programmed cell death · 2026
    Article
  4. The Significance of CXCL1 in Cancer: An Overview of Molecular Mechanisms.International journal of molecular sciences · 2026
    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

8 authors at 2 institutions in 1 country.

Biyin ChenDepartment of Oncology, The Third Affiliated People's Hospital of Fujian University of Traditional Chinese Medicine, Fuzhou, China.
Li SongDepartment of Oncology, The Third Affiliated People's Hospital of Fujian University of Traditional Chinese Medicine, Fuzhou, China.
Xiuzhen NieDepartment of Oncology, The Third Affiliated People's Hospital of Fujian University of Traditional Chinese Medicine, Fuzhou, China.
Fangfeng LinDepartment of Oncology, The Third Affiliated People's Hospital of Fujian University of Traditional Chinese Medicine, Fuzhou, China.
Zongyang YuDepartment of Pulmonary and Critical Care Medicine, The 900th Hospital of Joint Logistic Support Force, PLA, Fuzhou, China.
Wencui KongDepartment of Pulmonary and Critical Care Medicine, The 900th Hospital of Joint Logistic Support Force, PLA, Fuzhou, China.
Xiaoyan QiDepartment of Oncology, Zibo Central Hospital, Zibo, China.
Wenwu WangDepartment of Oncology, The Third Affiliated People's Hospital of Fujian University of Traditional Chinese Medicine, Fuzhou, China.
Fujian University of Traditional Chinese Medicine · CNCentral Hospital of Zibo · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeThis study made a systemic description for the CXCL1-dependent regulatory mechanism in colorectal cancer (CRC).

methodsBioinformatics methods were applied to obtain target mRNA CXCL1 and corresponding upstream miRNA. qRT-PCR and Western blot were performed to measure the levels of CXCL1 and miR-302e in CRC tissue and cells. Experiments including CCK-8, wound healing assay, Transwell invasion assay, and flow cytometry were conducted to assess cell biological behaviors. Dual-luciferase reporter assay was carried out for verification of the targeting relationship between CXCL1 and miR-302e. The inhibitor AG490 of JAK-STAT signaling pathway was used to identify the functional mechanism of CXCL1/JAK-STAT underlying progression of CRC, and tumor xenograft experiments were performed for further validation.

resultsCXCL1 was highly expressed in CRC tissue and cells, while miR-302e was poorly expressed. Silencing CXCL1 or overexpressing miR-302e could lead to inhibition of cell proliferation, migration, invasion but promotion of cell apoptosis of CRC. Besides, CXCL1 was identified as a direct target of miR-302e, and CXCL1 could reverse the effect of miR-302e on cell proliferation, migration, invasion, and apoptosis. Furthermore, CXCL1 functioned on CRC cell biological behaviors

conclusionCXCL1 could be regulated by miR-302e to inactivate JAK-STAT signaling pathway, in turn affecting cell proliferation, migration, invasion, and apoptosis of CRC. Our result provides a potential therapeutic target for CRC treatment.

Indexed as

chemokine ligand-1colorectal cancerjanus kinase signal transducer and activator of transcriptionmigration and invasionmiR-302eproliferation

Identifiers

PMID34079750
PMCPMC8166233
OpenAlexW3160242565

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.