Evidence map›Paper›PMID 32636645›Full record

ArticleOncoTargets and therapy2020

miR-335-5p Regulates Cell Cycle and Metastasis in Lung Adenocarcinoma by Targeting CCNB2.

Xiyong Wang, Huaiqing Xiao, Dongqiang Wu, Dongliang Zhang, Zhihao Zhang

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

44 citing papers in PubMed, 85 citations in OpenAlex.

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  5. GATA1 activates HSD17B6 to improve efficiency of cisplatin in lung adenocarcinoma via DNA damage.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2024
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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

5 authors at 1 institution.

Xiyong WangDepartment of Thoracic Surgery, China Coast Guard Hospital of the People's Armed Police Force, Jiaxing 314000, People's Republic of China.
Huaiqing XiaoDepartment of Thoracic Surgery, China Coast Guard Hospital of the People's Armed Police Force, Jiaxing 314000, People's Republic of China.
Dongqiang WuDepartment of Thoracic Surgery, China Coast Guard Hospital of the People's Armed Police Force, Jiaxing 314000, People's Republic of China.
Dongliang ZhangDepartment of Thoracic Surgery, China Coast Guard Hospital of the People's Armed Police Force, Jiaxing 314000, People's Republic of China.
Zhihao ZhangDepartment of Thoracic Surgery, China Coast Guard Hospital of the People's Armed Police Force, Jiaxing 314000, People's Republic of China.ORCID 0000-0003-0254-2113
Chinese People's Armed Police Force

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLots of studies have shown that cyclin disorders can promote tumor development. This study aims to investigate the biological function and molecular mechanism of CCNB2 in lung adenocarcinoma (LUAD).

methodsLUAD data were downloaded from GEO database and TCGA-LUAD database. Differential analysis was conducted to find the differentially expressed miRNAs and mRNAs, while targeted prediction was done for the access of potential target mRNAs. Gene expression level was detected by qRT-PCR and Western blot in human LUAD cell lines A-427, A549, Calu-3, PC-9 and human bronchial epithelial cell line BEAS-2B. MTT, colony formation, Transwell and flow cytometry assays were used to detect cell proliferation, metastasis, and cell cycle changes of PC-9 cell line. The dual-luciferase reporter gene was used to detect the targeted binding relationship of the target miRNA and mRNA.

resultsCCNB2 was highly expressed and served as a biomarker indicating poor prognosis in LUAD patients. Cell function experiments confirmed the inhibitory effects of silencing CCNB2 on the proliferation, migration and invasion of LUAD cells and cell cycle was blocked in the G0/G1 phase. In addition, with regard to the regulatory mechanism, we demonstrated that miR-335-5p had binding sites with 3'-UTR of CCNB2, indicating that miR-335-5p could target the regulation expression of CCNB2. In subsequent cell function tests, overexpression of miR-335-5p inhibited the proliferation and metastasis of cancer cells, and the rescue experiments also verified that miR-335-5p could reverse the promotion of CCNB2 overexpression on the progress of cancer cells.

conclusionIn summary, our results revealed that miR-335-5p could target the down-regulation of CCNB2 to inhibit the occurrence and development of LUAD.

Indexed as

CCNB2LUADmetastasismiR-335-5pproliferation

Identifiers

PMID32636645
PMCPMC7335273
OpenAlexW3037970867

What OpenQuestion holds

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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.