Evidence map›Paper›PMID 33023393›Full record

ArticleCancer biology & therapy2020

miR-221-3p promotes hepatocellular carcinogenesis by downregulating O6-methylguanine-DNA methyltransferase.

Zushun Chen, Bangde Xiang, Lunan Qi, Shaoliang Zhu, Lequn Li

Open access · bronzeAbstract read
In one paragraph

Article in Cancer biology & therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.0field-weighted citation impact, top 27% 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

15 citing papers in PubMed, 22 citations in OpenAlex.

  1. Role of non-coding RNAs in OOncology letters · 2026
    Review
  2. Article
  3. Genetic and epigenetic landscape of OExploration of targeted anti-tumor therapy · 2025
    Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. [MiR- 4719 inhibits migration and invasion of human breast cancer cells via targeting ARHGAP36].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2021
    Article
  14. Article
  15. 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

5 authors at 1 institution in 1 country.

Zushun ChenDepartment of Hepatobiliary Surgery, Guangxi Medical University Affiliated Tumor Hospital , Nanning, Guangxi, China.
Bangde XiangDepartment of Hepatobiliary Surgery, Guangxi Medical University Affiliated Tumor Hospital , Nanning, Guangxi, China.
Lunan QiDepartment of Hepatobiliary Surgery, Guangxi Medical University Affiliated Tumor Hospital , Nanning, Guangxi, China.
Shaoliang ZhuDepartment of Hepatobiliary Surgery, Guangxi Medical University Affiliated Tumor Hospital , Nanning, Guangxi, China.
Lequn LiDepartment of Hepatobiliary Surgery, Guangxi Medical University Affiliated Tumor Hospital , Nanning, Guangxi, China.
Tumor Hospital of Guangxi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study aimed to investigate the influence of miR-221-3p and O Fluorescence qPCR and immunoblot assays were performed to determine the expression of RNA and protein in HCC tissues and cell lines. We also employed the firefly and Renilla luciferase assay to verify the target relationship between miR-221-3p and MGMT mRNA. Assessments including the MTT assay, wound-healing assay, transwell assay, colony foci formation experiment, and flow cytometric experiment were carried out to determine the viability, migration, invasion, proliferation, cell cycle progression, and apoptosis of SMMC-7721 and BEL-7404 cell lines with the modulated expression of miR-221-3p and MGMT. Compared to healthy tissues and cell line HL7702, miR-221-3p was significantly upregulated but MGMT was significantly downregulated in carcinomas and cancerous cell lines. Forced miR-221-3p overexpression was found to enhance the proliferation, migration, invasion, and clonogenicity of cell lines, but it suppressed cell apoptosis. Findings also revealed that forced miR-221-3p overexpression had little effect on cell cycle progression. After MGMT was confirmed to be atarget gene of miR-221-3p, it was found that the forced upregulation of miR-221-3p downregulated MGMT mRNA and protein levels significantly. MiR-221-3p was identified as an HCC promoting factor, and it specifically inhibited the expression of the MGMT. Besides, the upregulation of miR-221-3p had apositive influence on HCC pathogenesis by inhibiting MGMT expression.

Indexed as

ApoptosisCarcinoma, HepatocellularCell ProliferationDNA Modification MethylasesDNA Repair EnzymesDown-RegulationHumansLiver NeoplasmsMicroRNAsTransfectionTumor Suppressor ProteinsDNA Modification MethylasesDNA Repair EnzymesMGMT protein, humanMicroRNAsMIR221, humanTumor Suppressor Proteinshepatocellular carcinomaMGMTmiR-221-3p

Identifiers

PMID33023393
PMCPMC7644250
OpenAlexW3092525494

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.