Evidence map›Paper›PMID 32286127›Full record

ArticleCell cycle (Georgetown, Tex.)2020

miR-206 inhibits liver cancer stem cell expansion by regulating EGFR expression.

Caifeng Liu, Jun Li, Wei Wang, Xingyang Zhong, Feng Xu, Junhua Lu

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

30 citing papers in PubMed, 42 citations in OpenAlex.

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  17. Non-Coding RNA Related to MAPK Signaling Pathway in Liver Cancer.International journal of molecular sciences · 2022
    Review
  18. Review
  19. MiR-206 improves intervertebral disk degeneration by targeting GJA1.Journal of orthopaedic surgery and research · 2022
    Article
  20. Frontiers in pharmacology · 2022
    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

6 authors at 1 institution in 1 country.

Caifeng LiuDepartment of Hepatic Surgery, Third Affiliated Hospital of Second Military Medical University, Shanghai, China.
Jun LiDepartment of Hepatic Surgery, Third Affiliated Hospital of Second Military Medical University, Shanghai, China.
Wei WangDepartment of Otolaryngology-Head & Neck Surgery, First Affiliated Hospital of Second Military Medical University, Shanghai, China.
Xingyang ZhongDepartment of Hepatic Surgery, Third Affiliated Hospital of Second Military Medical University, Shanghai, China.
Feng XuDepartment of Hepatic Surgery, Third Affiliated Hospital of Second Military Medical University, Shanghai, China.
Junhua LuDepartment of Hepatic Surgery, Third Affiliated Hospital of Second Military Medical University, Shanghai, China.
Second Military Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Liver cancer stem cells (CSCs) are involved in tumorigenesis, progression, drug resistance and recurrence of hepatocellular carcinoma (HCC). However, the underlying mechanism for the propagation of liver cancer stem cells was unclear. Herein, we observed miR-206 expression was reduced in both chemoresistant HCCs and recurrent HCCs from patients. A dramatically decrease of miR-206 was detected in cluster of differentiation 133 (CD133) or epithelial cell adhesion molecule (EpCAM)-positive liver CSCs and in CSC-enriched hepatoma spheres. Functional studies revealed that a forced expression of miR-206 inhibited liver CSCs expansion by suppressing the dedifferentiation of hepatoma cells and attenuating the self-renewal of liver CSCs. Mechanistically, bioinformatic and luciferase reporter analysis identified epidermal growth factor receptor (EGFR) as a direct target of miR-206. Moreover, miR-206 downregulated the expression of EGFR in liver CSCs. There was a significant inverse correlation between miR-206 and EGFR mRNA expression in HCC samples. Special EGFR inhibitor Gefitinib abolished the discrepancy in liver CSC proportion and the self-renewal capacity between miR-206 overexpression hepatoma cells and control cells, which further confirmed that EGFR was required in miR-206-inhibited liver CSCs expansion. Conclusion: miR-206 could suppress HCC cell dedifferentiation and liver CSCs expansion by targeting EGFR signaling.

Indexed as

ApoptosisBiomarkers, TumorCarcinogenesisCarcinoma, HepatocellularCell DedifferentiationCell Self RenewalDown-RegulationDrug Resistance, NeoplasmErbB ReceptorsGefitinibHep G2 CellsHumansLiver NeoplasmsMicroRNAsNeoplastic Stem CellsSignal TransductionBiomarkers, TumorEGFR protein, humanErbB ReceptorsGefitinibMicroRNAsMIRN206 microRNA, humandrug resistanceEGFRHepatocellular carcinomaliver cancer stem cellmiR-206

Identifiers

PMID32286127
PMCPMC7217366
OpenAlexW3015572430

What OpenQuestion holds

Textmetadata
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.