Evidence map›Paper›PMID 32897198›Full record

ArticleNan fang yi ke da xue xue bao = Journal of Southern Medical University2020

[Over-expression of miR-144 inhibits invasion of liver cancer SMMC-7721 cells

Qingsong Yi, Jiujiu Liu, Kurban Alexia, Jing Li, Hongwu Luo, Jichun Sun

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nan fang yi ke da xue xue bao = Journal of Southern Medical University, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.1field-weighted citation impact, top 61% of its field
1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

Who cites it

0 citing papers in PubMed, 1 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

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5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Qingsong YiDepartment of Hepatobiliary Surgery, Xiangya Third Hospital of Central South University, Changsha 410006, China.
Jiujiu LiuDepartment of Hepatobiliary Surgery, Xiangya Third Hospital of Central South University, Changsha 410006, China.
Kurban AlexiaDepartment of Hepatobiliary Surgery, Xiangya Third Hospital of Central South University, Changsha 410006, China.
Jing LiDepartment of Hepatobiliary Surgery, Xiangya Third Hospital of Central South University, Changsha 410006, China.
Hongwu LuoDepartment of Hepatobiliary Surgery, Xiangya Third Hospital of Central South University, Changsha 410006, China.
Jichun SunDepartment of Hepatobiliary Surgery, Xiangya Third Hospital of Central South University, Changsha 410006, China.
Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo investigate the effects of over-expression of miR-144 on invasion of SMMC-7721 cells and Toll-like receptor (TLR)/myeloid differentiation factor 88 (MyD88) pathway in hepatocellular carcinoma cells.

methodsThe expressions of miR-144 was examined in normal human hepatocyte line HL-7702 and hepatocarcinoma cell line SMMC-7721 using realtime quantitative PCR (qRT-PCR). SMMC-7721 cells were divided into blank group, miR-144 NC group and miR-144 mimics group, and the expressions of miR-144 in each group were detected with qRT-PCR. Cell count kit-8 (CCK8) was used to assess the survival of SMMC-7721 cells, and the cell invasion was evaluated using Transwell assay. The expressions of matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-9 (MMP-9) and TLR/MyD88 pathway-related proteins in the cells were detected with Western blotting; the effect of 40 μ mol/L MyD88 inhibitor on TLR/MyD88 pathway-related proteins was examined in SMMC-7721 cells.

resultsCompared with normal human hepatocytes, SMMC-7721 cells expressed a significantly lower level of miR-144 (

conclusionsOverexpression of miR-144 decreases SMMC-7721 cell survival and invasion by inhibiting TLR/MyD88 pathway.

Indexed as

Liver NeoplasmsCell Line, TumorHumansMatrix Metalloproteinase 2MicroRNAsMyeloid Differentiation Factor 88NF-kappa BSignal TransductionToll-Like ReceptorsMatrix Metalloproteinase 2MicroRNAsMIRN144 microRNA, humanMMP2 protein, humanMYD88 protein, humanMyeloid Differentiation Factor 88NF-kappa BToll-Like ReceptorsinvasionmiR-144SMMC-7721 cellssurvivalToll-like receptor/myeloid differentiation factor 88

Identifiers

PMID32897198
PMCPMC7277303
OpenAlexW3083945116

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.