Evidence map›Paper›PMID 32968445›Full record

ArticleOncology letters2020

MicroRNA-3690 promotes cell proliferation and cell cycle progression by altering DKK3 expression in human thyroid cancer.

Fei Shen, Xiao-Xiong Gan, Xing-Yan Deng, Jian-Hua Feng, Wen-Song Cai, Liang Shen, Huan-Qing Xiao, Bo Xu

Open access · diamondAbstract read
In one paragraph

Article in Oncology letters, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.6field-weighted citation impact, top 38% 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

7 citing papers in PubMed, 10 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
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 at 3 institutions in 1 country.

Fei ShenDepartment of Thyroid Surgery, Guangzhou First People's Hospital, Guangzhou Medical University, Guangzhou, Guangdong 510180, P.R. China.
Xiao-Xiong GanDepartment of Thyroid Surgery, Guangzhou First People's Hospital, Guangzhou Medical University, Guangzhou, Guangdong 510180, P.R. China.
Xing-Yan DengDepartment of Thyroid Surgery, Guangzhou First People's Hospital, Guangzhou Medical University, Guangzhou, Guangdong 510180, P.R. China.
Jian-Hua FengDepartment of Thyroid Surgery, Guangzhou First People's Hospital, Guangzhou Medical University, Guangzhou, Guangdong 510180, P.R. China.
Wen-Song CaiDepartment of Thyroid Surgery, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangzhou, Guangdong 510180, P.R. China.
Liang ShenDepartment of Thyroid Surgery, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangzhou, Guangdong 510180, P.R. China.
Huan-Qing XiaoDepartment of Thyroid Surgery, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangzhou, Guangdong 510180, P.R. China.
Bo XuDepartment of Thyroid Surgery, Guangzhou First People's Hospital, Guangzhou Medical University, Guangzhou, Guangdong 510180, P.R. China.
Guangzhou First People's Hospital · CNGuangzhou Medical University · CNSouth China University of Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

An increasing amount of evidence has demonstrated the importance of microRNAs (miRNAs/miRs) in the tumorigenesis of malignant types of cancer, and data retrieved from The Cancer Genome Atlas database revealed that miR-3690 was upregulated in thyroid cancer (TC). The present study focused on the biological function and mechanism of miR-3690 in TC, demonstrating that miR-3690 expression was significantly elevated in TC cells and clinical tissues. Functional studies indicated that miR-3690 acted as an oncogene in TC by promoting cell proliferation, colony formation and cell cycle progression in association with the increased expression of cyclin E and c-myc. Mechanistically, prediction software indicated that Dickkopf-related protein 3 (DKK3) was a target of miR-3690, which was confirmed by the results of luciferase reporter assays and western blotting. DKK3 silencing abrogated the functions of miR-3690-in on TC cell proliferation. Collectively, the findings of the present study demonstrated that miR-3690 promoted TC cell proliferation and indicated miR-3690 as a potential biomarker and therapeutic target for TC.

Indexed as

cell proliferationDickkopf-related protein 3human thyroid cancermicroRNA-3690the cell cycle

Identifiers

PMID32968445
PMCPMC7500009
OpenAlexW3084027630

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.