Evidence map›Paper›PMID 32130678›Full record

ArticleHuman cell2020

MiR-1256 inhibits cell proliferation and cell cycle progression in papillary thyroid cancer by targeting 5-hydroxy tryptamine receptor 3A.

Chaowen Wu, Liyuan Ma, Hongfa Wei, Furong Nie, Jie Ning, Tao Jiang

Abstract read
PubMed Publisher
In one paragraph

Article in Human cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

16 citing papers in PubMed, 24 citations in OpenAlex.

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  14. Eight Differential miRNAs in DN Identified by Microarray Analysis as Novel Biomarkers.Diabetes, metabolic syndrome and obesity : targets and therapy · 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

6 authors at 3 institutions in 1 country.

Chaowen Wu *Department of Metabolic Endocrinology, Shenzhen Longhua District Central Hospital, No. 187 Guanlan Avenue, Longhua District, Shenzhen, 518110, China.
Liyuan Ma *Department of Ultrasound, General Hospital of Ningxia Medical University, Yinchuan, 750004, China.
Hongfa WeiDepartment of Metabolic Endocrinology, Shenzhen Longhua District Central Hospital, No. 187 Guanlan Avenue, Longhua District, Shenzhen, 518110, China.
Furong NieDepartment of Metabolic Endocrinology, Shenzhen Longhua District Central Hospital, No. 187 Guanlan Avenue, Longhua District, Shenzhen, 518110, China.
Jie NingDepartment of Metabolic Endocrinology, Shenzhen Longhua District Central Hospital, No. 187 Guanlan Avenue, Longhua District, Shenzhen, 518110, China. ningjiejie23wk@2980.com.
Tao JiangDepartment of Anal-Colorectal Surgery, General Hospital of Ningxia Medical University, No. 804 South Shengli Road, Yinchuan, 750004, China. taojiang_0304@126.com.
Longgang Central Hospital · CNNingxia Medical University · CNNingxia Medical University General Hospital · CN

Funding

National Natural Science Foundation of China 81560394Natural Science Foundation of Ningxia 2018AAC03131Science and Technology Innovation Fund Project in Longhua District of Shenzhen City 20150827A0410012, 20150826A1030068, JCYJ20160428141615317Scientific Research Project grant funded by Ningxia High School NGY2018-76
6 · The paper itself

Abstract

Aberrant expression of miR-1256 has been reported to be closely associated with the development and progression of tumors, including colon cancer and lung cancer. However, study of its expression pattern and functional role in papillary thyroid cancer (PTC) is rare. Using quantitative real time PCR analysis, we found miR-1256 was significantly down-regulated in PTC tissues and cell lines. The correlation of miR-1256 expression with clinicopathological features was statistically analyzed. The results showed miR-1256 expression was significantly correlated with tumor size (p = 0.0124) and TNM stage (p = 0.0032). Restoring miR-1256 expression significantly inhibited proliferation and cell cycle progression of PTC cells demonstrated by CCK-8 and flow cytometry assays. Luciferase reporter assay and biotin-avidin pull-down assay showed miR-1256 can directly target 5-hydroxytryptamine receptor 3A (HTR3A) in PTC cells. The expression of miR-1256 was inversely correlated with HTR3A expression in PTC tissues. Knockdown of HTR3A imitated the suppressive effects of miR-1256 in PTC cells. Ectopic expression of HTR3A can antagonize the effects of miR-1256 on PTC cells. Furthermore, the suppressive effects of miR-1256 on the expression of PCNA, CDK4, Cyclin D1, and p21 were partially reversed by HTR3A overexpression in PTC cells. In summary, our data suggested that miR-1256 could suppress PTC cellular function by targeting HTR3A, which might be a potential therapeutic target for patients with PTC.

Indexed as

Cell CycleCell ProliferationHumansMicroRNAsMolecular Targeted TherapyThyroid Cancer, PapillaryThyroid NeoplasmsTumor Cells, CulturedMicroRNAsMIRN1256 microRNA, humanCell cycleCell proliferationHTR3AmiR-1256Papillary thyroid cancer

Identifiers

PMID32130678
OpenAlexW3009687828

What OpenQuestion holds

Textmetadata
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.