Evidence map›Paper›PMID 27313460›Full record

ArticleOncoTargets and therapy2016

Restoration of miR-20a expression suppresses cell proliferation, migration, and invasion in HepG2 cells.

Guang Shun Chen, Ning Zhou, Jie-Qun Li, Ting Li, Zhong-Qiang Zhang, Zhong-Zhou Si

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

7 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. LncRNA UCC promotes epithelial-mesenchymal transition via the miR-143-3p/SOX5 axis in non-small-cell lung cancer.Laboratory investigation; a journal of technical methods and pathology · 2021
    Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Upregulation of miR-129-5p increases the sensitivity to Taxol through inhibiting HMGB1-mediated cell autophagy in breast cancer MCF-7 cells.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2019
    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 2 institutions in 1 country.

Guang Shun ChenDepartment of Organ Transplantation and General Surgery, The Second Xiangya Hospital, Central South University, Changsha, People's Republic of China.
Ning ZhouDepartment of Organ Transplantation and General Surgery, The Second Xiangya Hospital, Central South University, Changsha, People's Republic of China.
Jie-Qun LiDepartment of Organ Transplantation and General Surgery, The Second Xiangya Hospital, Central South University, Changsha, People's Republic of China.
Ting LiDepartment of Organ Transplantation and General Surgery, The Second Xiangya Hospital, Central South University, Changsha, People's Republic of China.
Zhong-Qiang ZhangDepartment of Organ Transplantation and General Surgery, The Second Xiangya Hospital, Central South University, Changsha, People's Republic of China.
Zhong-Zhou SiDepartment of Organ Transplantation and General Surgery, The Second Xiangya Hospital, Central South University, Changsha, People's Republic of China.
Second Xiangya Hospital of Central South University · CNCentral South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo study microRNA (miR)-20a expression in hepatocellular carcinoma (HCC) and its effects on the proliferation, migration, and invasion of HepG2.

methodsThe real-time polymerase chain reaction was used to detect the expression of miR-20a in HCC tissue and normal tissue, as well as in HCC cell lines and normal liver cells. miR-20a mimic and miR negative control (NC) were transfected into HepG2 cells. MTT (3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide) assay was used to detect cell proliferation. Annexin fluorescein isothiocyanate/propidium iodide assay was run to examine the early apoptosis of cells. Transwell chamber assay was carried out to investigate the cell invasion and migration abilities.

resultsmiR-20a was lowly expressed both in HCC tissues and HCC cell lines. After transfection of exogenous miR-20 mimics, miR-20a expression in HepG2 cells was significantly increased by 61.29% compared to the blank group (P<0.01). MTT assay showed that the growth of HepG2 cells in the miR-20a mimics group was significantly inhibited, and optical density values during the 36-96 hour time period were dramatically decreased compared to the blank group (P<0.01). Apoptosis rates of the miR-20a mimics group were higher than those of the blank and NC groups (both P<0.01). The number of HCC cells after transfection by miR-20a mimics in the G1 and S phases were 15.88% and 7.89%, respectively, which were lower than in the blank and NC groups (both P<0.05). Transwell assay showed that in the miR-20a mimics group the number of cell migration and invasion were 0.459 and 0.501 times that of the blank group (both P<0.01), and the migration and inhibition rates were 54.1% and 51.4%, respectively. After closing target gene CCND1 in HepG2 cells, the number of cell migration and invasion in the small interfering (si)-CCND1 group were 0.444 and 0.435 times that of the si-NC group (P<0.05); and compared to the si-NC group, the migration and inhibition rates were 55.6% and 56.5%, respectively.

conclusionmiR-20a can inhibit the growth, invasion, and migration of HepG2 cells, and is therefore promising as a new molecular target for diagnosis and therapy of HCC.

Indexed as

HepG2 cellsinvasionmigrationmiR-20aproliferation

Identifiers

PMID27313460
PMCPMC4892835
OpenAlexW2395806022

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.