Evidence map›Paper›PMID 33723215›Full record

ArticleCell death & disease2021

FoxP3-miR-150-5p/3p suppresses ovarian tumorigenesis via an IGF1R/IRS1 pathway feedback loop.

Qinkai Zhang, Xunzhu Zhou, Maoping Wan, Xixi Zeng, Jiarong Luo, Yesha Xu, Liying Ji, Jian-An Zhang, Pei Fan, Jianing Zhong and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

23 citing papers in PubMed, 29 citations in OpenAlex.

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  20. Computational and mathematical methods in medicine · 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

11 authors at 2 institutions in 1 country.

Qinkai Zhang *Institute of Genomic Medicine, Wenzhou Medical University, Wenzhou, Zhejiang, P.R. China.
Xunzhu Zhou *Institute of Genomic Medicine, Wenzhou Medical University, Wenzhou, Zhejiang, P.R. China.
Maoping Wan *Institute of Genomic Medicine, Wenzhou Medical University, Wenzhou, Zhejiang, P.R. China.
Xixi ZengInstitute of Genomic Medicine, Wenzhou Medical University, Wenzhou, Zhejiang, P.R. China.
Jiarong LuoInstitute of Genomic Medicine, Wenzhou Medical University, Wenzhou, Zhejiang, P.R. China.
Yesha XuInstitute of Genomic Medicine, Wenzhou Medical University, Wenzhou, Zhejiang, P.R. China.
Liying JiInstitute of Genomic Medicine, Wenzhou Medical University, Wenzhou, Zhejiang, P.R. China.
Jian-An ZhangDepartment of Obstetrics and Gynecology, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, P.R. China.
Pei FanDepartment of Orthopedics, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, P.R. China.
Jianing ZhongKey Laboratory of Prevention and Treatment of Cardiovascular and Cerebrovascular Diseases, Ministry of Education, Gannan Medical University, Ganzhou, Jiangxi, P.R. China. zhongning_003@163.com.ORCID 0000-0002-2781-3437
Jianmin WuInstitute of Genomic Medicine, Wenzhou Medical University, Wenzhou, Zhejiang, P.R. China. Jianminwu81@hotmail.com.ORCID 0000-0002-8223-1667
Wenzhou Medical University · CNGannan Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ovarian cancer (OC) causes more deaths than any other gynecological cancer. Many cellular pathways have been elucidated to be associated with OC development and progression. Specifically, the insulin-like growth factor 1 receptor/insulin receptor substrate 1 (IGF1R/IRS1) pathway participates in OC development. Moreover, accumulating evidence has shown that microRNA deregulation contributes to tumor initiation and progression. Here, our study aimed to investigate the molecular functions and regulatory mechanisms of miR-150, specifically, in OC. We found that the expression of miR-150-5p/3p and their precursor, mir-150, was downregulated in OC tissues; lower mir-150 levels were associated with poor OC patient outcomes. Ectopic mir-150 expression inhibited OC cell growth and metastasis in vitro and in vivo. Furthermore, both IRS1 and IGF1R were confirmed as direct targets of miR-150-5p/3p, and the miR-150-IGF1R/IRS1 axis exerted antitumor effects via the PI3K/AKT/mTOR pathway. Forkhead box protein 3 (FoxP3) positively regulated the expression of miR-150-5p/3p by binding to the mir-150 promoter. In turn, the PI3K/AKT/mTOR pathway downregulated FoxP3 and miR-150-5p/3p. Taken together, these findings indicate that a complex FoxP3-miR-150-IGF1R/IRS1-PI3K/AKT/mTOR feedback loop regulates OC pathogenesis, providing a novel mechanism for miR-150 as a tumor suppressor miRNA in OC.

Indexed as

Cell MovementCell ProliferationAnimalsApoptosisCell Line, TumorFeedback, PhysiologicalFemaleForkhead Transcription FactorsGene Expression Regulation, NeoplasticHEK293 CellsHumansInsulin Receptor Substrate ProteinsMiceMice, Inbred BALB CMice, NudeMicroRNAsForkhead Transcription FactorsFOXP3 protein, humanIGF1R protein, humanInsulin Receptor Substrate ProteinsIRS1 protein, humanMicroRNAsMIR150, humanMTOR protein, humanPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktReceptor, IGF Type 1TOR Serine-Threonine Kinases

Identifiers

PMID33723215
PMCPMC7961150
OpenAlexW3139488613

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.