Evidence map›Paper›PMID 25889562›Full record

ArticleMolecular cancer2015

Down-regulation of miR-675-5p contributes to tumor progression and development by targeting pro-tumorigenic GPR55 in non-small cell lung cancer.

Dan He, Jun Wang, Chunfang Zhang, Bin Shan, Xiyun Deng, Bin Li, Yanwu Zhou, Wei Chen, Jidong Hong, Yang Gao and 2 more

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

64 citing papers in PubMed, 90 citations in OpenAlex.

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  14. LncRNAInternational journal of molecular sciences · 2021
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  20. Review

4 more citing papers are in PubMed but not listed here.

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

12 authors at 4 institutions in 2 countries.

Dan HeKey Laboratory of Cancer Proteomics of Chinese Ministry of Health, Institute of Medical Sciences, Xiangya Hospital, Central South University, Xiangya Road 87th, Changsha, 410008, Hunan, PR China. 714151179@qq.com.
Jun WangKey Laboratory of Cancer Proteomics of Chinese Ministry of Health, Institute of Medical Sciences, Xiangya Hospital, Central South University, Xiangya Road 87th, Changsha, 410008, Hunan, PR China. 768735234@qq.com.
Chunfang ZhangKey Laboratory of Cancer Proteomics of Chinese Ministry of Health, Institute of Medical Sciences, Xiangya Hospital, Central South University, Xiangya Road 87th, Changsha, 410008, Hunan, PR China. zcf6636169@sina.com.
Bin ShanCollege of Medical Sciences, Washington State University Spokane, 412 E.Spokane Falls Boulevard, Spokane, WA, 99202, USA. bin.shan@wsu.edu.
Xiyun DengFaculty of Basic Medical Sciences, College of Medicine, Hunan Normal University, Changsha, 410013, PR China. dengxiyunmed@hunnu.edu.cn.
Bin LiKey Laboratory of Cancer Proteomics of Chinese Ministry of Health, Institute of Medical Sciences, Xiangya Hospital, Central South University, Xiangya Road 87th, Changsha, 410008, Hunan, PR China. lb930336@163.com.
Yanwu ZhouKey Laboratory of Cancer Proteomics of Chinese Ministry of Health, Institute of Medical Sciences, Xiangya Hospital, Central South University, Xiangya Road 87th, Changsha, 410008, Hunan, PR China. zhouyanwudream@163.com.
Wei ChenKey Laboratory of Cancer Proteomics of Chinese Ministry of Health, Institute of Medical Sciences, Xiangya Hospital, Central South University, Xiangya Road 87th, Changsha, 410008, Hunan, PR China. 1375266291@qq.com.
Jidong HongKey Laboratory of Cancer Proteomics of Chinese Ministry of Health, Institute of Medical Sciences, Xiangya Hospital, Central South University, Xiangya Road 87th, Changsha, 410008, Hunan, PR China. hongjidong1966@126.com.
Yang GaoKey Laboratory of Cancer Proteomics of Chinese Ministry of Health, Institute of Medical Sciences, Xiangya Hospital, Central South University, Xiangya Road 87th, Changsha, 410008, Hunan, PR China. gaoyang_george@sina.com.
Zhuchu ChenKey Laboratory of Cancer Proteomics of Chinese Ministry of Health, Institute of Medical Sciences, Xiangya Hospital, Central South University, Xiangya Road 87th, Changsha, 410008, Hunan, PR China. chenzhuchu@126.com.
Chaojun DuanKey Laboratory of Cancer Proteomics of Chinese Ministry of Health, Institute of Medical Sciences, Xiangya Hospital, Central South University, Xiangya Road 87th, Changsha, 410008, Hunan, PR China. duancjxy@126.com.
Central South University · CNXiangya Hospital Central South University · CNHunan Normal University · CNWashington State University Spokane · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundmicroRNAs are small noncoding RNAs that modulate a variety of cellular processes by regulating multiple targets, which can promote or inhibit the development of malignant behaviors. Accumulating evidence suggests that miR-675-5p plays important roles in human carcinogenesis. However, its precise biological role remains largely elusive. This study examined the role of miR-675-5p in non- small cell lung cancer (NSCLC).

methodsThe expression of miR-675-5p was analyzed by real-time quantitative PCR (qRT-PCR). The effect of miR-675-5p on proliferation was evaluated through MTT and colony formation assays, and cell migration and invasion were evaluated through transwell assays. The expression of target proteins and downstream molecules was analyzed by western blotting and immunohistochemical staining. The luciferase reporter assay was used to assess the target genes of miR-675-5p in non-small cell lung cancer cells.

resultsThe expression levels of miR-675-5p in NSCLC tissues were significantly reduced compared to those in adjacent non-cancerous tissues (P < 0.001). The expression of miR-675-5p in patients with non-small cell lung cancer had a negative correlation with lymph node metastasis (P < 0.01) and TNM stage (P < 0.05). Down-regulation of miR-675-5p promoted cell growth, proliferation, colony formation, invasion and migration, and promoted the tumorigenicity graft growth of nude mice in vivo (P < 0.01); whereas up-regulation of miR-675-5p had the contrary effects. The luciferase reporter assay showed that GPR55 was a direct target gene of miR-675-5p. Overexpression of miR-675-5p can lead to the down-regulation of GPR55 and its signaling pathway, whereas the effect can be reversed by down-regulation of miR-675-5p expression.

conclusionsmiR-675-5p functions as a novel tumor suppressor in NSCLC and the anti-oncogenic activity may involve its inhibition of the target gene GPR55. These findings suggest the possibility for miR-675-5p as a therapeutic target in NSCLC.

Indexed as

AnimalsCarcinogenesisCarcinoma, Non-Small-Cell LungCell Line, TumorCell MovementCell ProliferationDisease ProgressionDown-RegulationFemaleHumansLung NeoplasmsLymphatic MetastasisMaleMiceMice, NudeMicroRNAsGPR55 protein, humanMicroRNAsMIRN675 microRNA, humanReceptors, CannabinoidReceptors, G-Protein-Coupled

Identifiers

PMID25889562
PMCPMC4392735
OpenAlexW2163642215

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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.