Evidence map›Paper›PMID 30333561›Full record

ArticleCell death & disease2018

Down-regulation of HPGD by miR-146b-3p promotes cervical cancer cell proliferation, migration and anchorage-independent growth through activation of STAT3 and AKT pathways.

Shuihong Yao, Jingyun Xu, Kaixuan Zhao, Pengxia Song, Qin Yan, Weifei Fan, Wan Li, Chun Lu

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

39 citing papers in PubMed, 99 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Shuihong YaoState Key Laboratory of Reproductive Medicine, Nanjing Medical University, Nanjing, 211166, P. R. China.
Jingyun XuKey Laboratory of Pathogen Biology of Jiangsu Province, Nanjing Medical University, Nanjing, 211166, P. R. China.
Kaixuan ZhaoKey Laboratory of Pathogen Biology of Jiangsu Province, Nanjing Medical University, Nanjing, 211166, P. R. China.
Pengxia SongMedical School, Quzhou College of Technology, Quzhou, 324000, P. R. China.
Qin YanState Key Laboratory of Reproductive Medicine, Nanjing Medical University, Nanjing, 211166, P. R. China.
Weifei FanDepartment of Hematology and Oncology, Department of Geriatric Lung Cancer Research Laboratory, Geriatric Hospital of Nanjing Medical University, Nanjing, 210024, P. R. China. weifeifan1503@163.com.
Wan LiState Key Laboratory of Reproductive Medicine, Nanjing Medical University, Nanjing, 211166, P. R. China. wanli@njmu.edu.cn.
Chun LuState Key Laboratory of Reproductive Medicine, Nanjing Medical University, Nanjing, 211166, P. R. China. clu@njmu.edu.cn.
Nanjing Medical University · CNQuzhou College of Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

While the application of early screening and HPV vaccines has reduced the incidence and mortality rates of cervical cancer, it remains the third most common carcinoma and fourth leading cause of cancer-associated death among women worldwide. The precise mechanisms underlying progression of cervical cancer are not fully understood at present. Here, we detected significant down-regulation of 15-hydroxyprostaglandin dehydrogenase (HPGD) in cervical cancer tissues. Overexpression of HPGD inhibited cervical cancer cell proliferation, migration and anchorage-independent growth to a significant extent. To clarify the mechanisms underlying HPGD down-regulation in cervical cancer, miRNA microarray, bioinformatics and luciferase reporter analyses were performed. HPGD was identified as a direct target of miR-146b-3p displaying up-regulation in cervical cancer tissues. Similar to the effects of HPGD overexpression, down-regulation of miR-146b-3p strongly suppressed proliferation, migration and anchorage-independent growth of cervical cancer cells. Furthermore, HPGD negatively regulated activities of STAT3 and AKT that promote cervical cancer cell proliferation. Notably, HPV oncogenes E6 and E7 were determined as potential contributory factors to these alterations. Our results collectively suggest that the HPGD/miR-146b-3p axis plays a significant role in cervical cancer and may serve as a potentially effective therapeutic target.

Indexed as

Gene Expression Regulation, NeoplasticBase SequenceCell Line, TumorCell MovementCell ProliferationDisease ProgressionFemaleHEK293 CellsHeLa CellsHost-Pathogen InteractionsHuman papillomavirus 16Human papillomavirus 18HumansHydroxyprostaglandin DehydrogenasesMicroRNAsOncogene Proteins, Viral15-hydroxyprostaglandin dehydrogenaseE6 protein, Human papillomavirus type 16Hydroxyprostaglandin DehydrogenasesMicroRNAsMIRN146 microRNA, humanoncogene protein E7, Human papillomavirus type 16Oncogene Proteins, ViralPapillomavirus E7 ProteinsProto-Oncogene Proteins c-aktRepressor ProteinsSTAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID30333561
PMCPMC6192999
OpenAlexW2897234637

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.