Evidence map›Paper›PMID 30171257›Full record

ArticleOncogene2019

MicroRNA 483-3p targets Pard3 to potentiate TGF-β1-induced cell migration, invasion, and epithelial-mesenchymal transition in anaplastic thyroid cancer cells.

Xiaoping Zhang, Lin Liu, Xianzhao Deng, Dan Li, Haidong Cai, Yushui Ma, Chengyou Jia, Bo Wu, Youben Fan, Zhongwei Lv

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncogene, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

40 citing papers in PubMed, 54 citations in OpenAlex.

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  19. Dual Function of Par3 in Tumorigenesis.Frontiers in oncology · 2022
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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

10 authors at 4 institutions in 1 country.

Xiaoping ZhangDepartment of Nuclear Medicine, Shanghai Tenth People's Hospital, Tongji University, Shanghai, 200072, China.
Lin LiuDepartment of Nuclear Medicine, Shanghai Tenth People's Hospital, Tongji University, Shanghai, 200072, China.
Xianzhao DengCenter of Thyroid, Department of General Surgery, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, 200233, China.
Dan LiDepartment of Nuclear Medicine, Shanghai Tenth People's Hospital, Tongji University, Shanghai, 200072, China.
Haidong CaiDepartment of Nuclear Medicine, Shanghai Tenth People's Hospital, Tongji University, Shanghai, 200072, China.
Yushui MaDepartment of Nuclear Medicine, Shanghai Tenth People's Hospital, Tongji University, Shanghai, 200072, China.
Chengyou JiaDepartment of Nuclear Medicine, Shanghai Tenth People's Hospital, Tongji University, Shanghai, 200072, China.
Bo WuCenter of Thyroid, Department of General Surgery, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, 200233, China. wubo7421@sohu.com.
Youben FanCenter of Thyroid, Department of General Surgery, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, 200233, China. fanyouben2006@163.com.
Zhongwei LvDepartment of Nuclear Medicine, Shanghai Tenth People's Hospital, Tongji University, Shanghai, 200072, China. heyixue163@163.com.
Shanghai Tenth People's Hospital · CNTongji University · CNShanghai Jiao Tong University · CNShanghai Sixth People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Anaplastic thyroid cancer (ATC) is associated with poor prognosis and is often untreatable. MicroRNA 483-3p (miR-483) and partitioning-defective 3 (Pard3), a member of the Pard family, have functions and regulatory mechanisms in ATC. The abnormal regulation of miR-483 may play an important role in tumorigenesis, and Par3 is known to regulate cell polarity, cell migration, and cell division. Tumor proliferation promoted by the regulation of miRNA expression can be regulated in thyroid cancer by upregulating transforming growth factor-β1 (TGF-β1), which is thought to interact with Pard3. When compared with adjacent non-tumor tissues, we found that miR-483 was upregulated and Pard3 was downregulated in 80 thyroid tumor samples. Disease-free survival was decreased when expression of miR-483 was upregulated and Pard3 expression was downregulated. Cell growth, migration, and invasion were induced by overexpression of miR-483. However, knockdown of miR-483 resulted in a loss of cell invasion and viability, both in vitro and in vivo. The expression of Pard3 was increased by the inhibition of miR-483, but TGF-β1-induced cell migration and invasion were decreased by miR-483 inhibition. A dual-luciferase reporter assay determined that Pard3 expression was downregulated when targeted with miR-483. The epithelial-mesenchymal transition (EMT), as well as Tiam1-Rac signaling, was induced by TGF-β1, which was decreased by the overexpression of Pard3. Pard3 decreased the inhibition of EMT and Tiam-Rac1 signaling, which resulted from transfection of ATC cells with miR-483. Overall, the results showed that downregulation of Pard3 resulted in increased cell invasion and EMT in ATC, which was promoted by treatment with miR-483. These findings suggest novel therapeutic targets and treatment strategies for this disease.

Indexed as

Cell MovementEpithelial-Mesenchymal TransitionAdaptor Proteins, Signal TransducingAgedCell Cycle ProteinsCell Line, TumorFemaleGene Expression Regulation, NeoplasticHumansMaleMembrane ProteinsMicroRNAsMiddle AgedNeoplasm InvasivenessNeoplasm ProteinsRNA, NeoplasmAdaptor Proteins, Signal TransducingCell Cycle ProteinsMembrane ProteinsMicroRNAsMIRN483 microRNA, humanNeoplasm ProteinsPARD3 protein, humanRNA, NeoplasmTGFB1 protein, humanTransforming Growth Factor beta1

Identifiers

PMID30171257
PMCPMC6756112
OpenAlexW2888959026

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.