Evidence map›Paper›PMID 31925702›Full record

ArticleHuman cell2020

miR-362-5p promotes cell proliferation and cell cycle progression by targeting GAS7 in acute myeloid leukemia.

Fuqun Wu, Changxin Yin, Junhua Qi, Deyu Duan, Xi Jiang, Jianhua Yu, Zhaofan Luo

Open access · hybridAbstract read
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 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

19 citing papers in PubMed, 31 citations in OpenAlex.

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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

7 authors at 3 institutions in 1 country.

Fuqun WuDepartment of Clinical Laboratory, The Seventh Affiliated Hospital of Sun-Yat-Sen University, No. 628, Zhenyuan Road, Guangming District, Shenzhen, 518017, Guangdong, China. wu_fuqun1314@126.com.
Changxin YinDepartment of Hematology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, Guangdong, China.
Junhua QiDepartment of Clinical Laboratory, The Seventh Affiliated Hospital of Sun-Yat-Sen University, No. 628, Zhenyuan Road, Guangming District, Shenzhen, 518017, Guangdong, China.
Deyu DuanDepartment of Clinical Laboratory, The Seventh Affiliated Hospital of Sun-Yat-Sen University, No. 628, Zhenyuan Road, Guangming District, Shenzhen, 518017, Guangdong, China.
Xi JiangDepartment of Clinical Laboratory, The Seventh Affiliated Hospital of Sun-Yat-Sen University, No. 628, Zhenyuan Road, Guangming District, Shenzhen, 518017, Guangdong, China.
Jianhua YuDepartment of Hematology, Kanghua Hospital, Dongguan, 523080, Guangdong, China.
Zhaofan LuoDepartment of Hematology, Kanghua Hospital, Dongguan, 523080, Guangdong, China.
Guhua Hospital · CNSun Yat-sen University · CNNanfang Hospital · CN

Funding

Dongguan Science and Technology Project and A study on relationship between MLH1 gene mutation and prognosis of acute myeloid leukemia 201750715059034
6 · The paper itself

Abstract

Recently, miR-362-5p has attracted special interest as a novel prognostic predictor in acute myeloid leukemia (AML). However, its biological function and underlying molecular mechanism in AML remain to be further defined. Herein, we found that a significant increase in miR-362-5p expression was observed in AML patients and cell lines using quantitative real-time PCR. The expression of miR-362-5p was altered in THP-1 and HL-60 cells by transfecting with miR-362-5p mimic or inhibitor. A series of experiments showed that inhibition of miR-362-5p expression significantly suppressed cell proliferation, induced G0/G1 phase arrest and attenuated tumor growth in vivo. On the contrary, ectopic expression of miR-362-5p resulted in enhanced cell proliferation, cell cycle progression and tumor growth. Moreover, growth arrest-specific 7 (GAS7) was confirmed as a direct target gene of miR-362-5p and was negatively modulated by miR-362-5p. GAS7 overexpression imitated the tumor suppressive effect of silenced miR-362-5p on THP-1 cells. Furthermore, miR-362-5p knockdown or GAS7 overexpression obviously down-regulated the expression levels of PCNA, CDK4 and cyclin D1, but up-regulated p21 expression. Collectively, our findings demonstrate that miR-362-5p exerts oncogenic effects in AML by directly targeting GAS7, which might provide a promising therapeutic target for AML.

Indexed as

Nerve Tissue ProteinsCell Cycle CheckpointsCell ProliferationHumansLeukemia, Myeloid, AcuteMicroRNAsMolecular Targeted TherapyGAS7 protein, humanMicroRNAsMIRN362 microRNA, humanNerve Tissue ProteinsAcute myeloid leukemiaCell cycleGAS7miR-362-5p

Identifiers

PMID31925702
PMCPMC7080691
OpenAlexW2999761149

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.