Evidence map›Paper›PMID 29663730›Full record

ArticleCancer medicine2018

MiR-21 improves invasion and migration of drug-resistant lung adenocarcinoma cancer cell and transformation of EMT through targeting HBP1.

Chongyu Su, Xu Cheng, Yunsong Li, Yi Han, Xiaoyun Song, Daping Yu, Xiaoqing Cao, Zhidong Liu

Abstract read
In one paragraph

Article in Cancer medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
–field-weighted citation impact
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

29 citing papers in PubMed.

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  20. Regulation of PD-1/PD-L1 Pathway in Cancer by Noncoding RNAs.Pathology oncology research : POR · 2020
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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.

Chongyu SuDepartment of Thoracic Surgery, Beijing Chest Hospital, Capital Medical University, Beijing, 101149, China.
Xu ChengDepartment of Thoracic Surgery, Beijing Chest Hospital, Capital Medical University, Beijing, 101149, China.
Yunsong LiDepartment of Thoracic Surgery, Beijing Chest Hospital, Capital Medical University, Beijing, 101149, China.
Yi HanDepartment of Thoracic Surgery, Beijing Chest Hospital, Capital Medical University, Beijing, 101149, China.
Xiaoyun SongDepartment of Thoracic Surgery, Beijing Chest Hospital, Capital Medical University, Beijing, 101149, China.
Daping YuDepartment of Thoracic Surgery, Beijing Chest Hospital, Capital Medical University, Beijing, 101149, China.
Xiaoqing CaoDepartment of Thoracic Surgery, Beijing Chest Hospital, Capital Medical University, Beijing, 101149, China.
Zhidong LiuDepartment of Thoracic Surgery, Beijing Chest Hospital, Capital Medical University, Beijing, 101149, China.ORCID 0000-0002-5622-4228

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study was aimed at the investigation of the effects of miR-21 on drug resistance, invasion, migration, and epithelial-mesenchymal transition (EMT) of lung adenocarcinoma cells and the related molecular mechanisms. Cell viability of A549 cell line was measured by MTT assay. Wound healing assay and transwell assay were, respectively, employed to examine cell migration and invasion abilities. The cells were transfected with miR-21 mimic or inhibitor using Lipofectamine 3000. The target relationship between miR-21 and HBP1 was confirmed by luciferase reporter gene assay. Western blot and qRT-PCR were used to examine the expression of HBP1 and EMT-related molecules. Compared with A549 cells, drug resistance of A549/PTX cells and A549/DDP cells were obviously stronger. A549/PTX cells and A549/DDP cells had stronger ability of migration and invasion compared with parental A549 cells. Meanwhile, EMT of A549/PTX and A549/DDP was significantly higher than that of A549 cells. MiR-21 promoted migration, invasion, and EMT of human lung adenocarcinoma cancer cells. Our experiment also verified the target relationship between miR-21 and HBP1. MiR-21 may affect migration and invasion ability of drug-resistant lung adenocarcinoma cells by targeting HBP1, therefore modulating EMT.

Indexed as

3' Untranslated RegionsAdenocarcinoma of LungCell Line, TumorCell MovementCell SurvivalCisplatinDose-Response Relationship, DrugDrug Resistance, NeoplasmEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHigh Mobility Group ProteinsHumansMicroRNAsModels, BiologicalRepressor ProteinsRNA Interference3' Untranslated RegionsCisplatinHBP1 protein, humanHigh Mobility Group ProteinsMicroRNAsMIRN21 microRNA, humanRepressor ProteinsDrug resistanceepithelial-mesenchymal transitionHBP1lung adenocarcinomamiRNA-21

Identifiers

PMID29663730
PMCPMC6010699

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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.