Evidence map›Paper›PMID 27095304›Full record

ArticleNature communications2016

miR-3188 regulates nasopharyngeal carcinoma proliferation and chemosensitivity through a FOXO1-modulated positive feedback loop with mTOR-p-PI3K/AKT-c-JUN.

Mengyang Zhao, Rongcheng Luo, Yiyi Liu, Linyuan Gao, Zhaojian Fu, Qiaofen Fu, Xiaojun Luo, Yiyu Chen, Xiaojie Deng, Zixi Liang and 4 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 113 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
113citing papers in PubMed, 1 pooled it
13.2field-weighted citation impact, top 1% 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

113 citing papers in PubMed, 1 synthesis or guideline pooled it, 163 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
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  5. Review
  6. Article
  7. Article
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  11. Non-Muscle Myosin II A: Friend or Foe in Cancer?International journal of molecular sciences · 2024
    Review
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  13. Review
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  15. Article
  16. METTL3 Mediates Epithelial-Mesenchymal Transition by Modulating FOXO1 mRNA NAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Article
  17. Article
  18. Review
  19. Review
  20. Article

53 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 3 institutions in 1 country.

Mengyang ZhaoCancer Center, Traditional Chinese Medicine-Integrated Hospital, Southern Medical University, Guangzhou 510315, China.
Rongcheng LuoCancer Center, Traditional Chinese Medicine-Integrated Hospital, Southern Medical University, Guangzhou 510315, China.
Yiyi LiuCancer Research Institute, Southern Medical University, Guangzhou 510515, China.
Linyuan GaoCancer Research Institute, Southern Medical University, Guangzhou 510515, China.
Zhaojian FuCancer Research Institute, Southern Medical University, Guangzhou 510515, China.
Qiaofen FuCancer Research Institute, Southern Medical University, Guangzhou 510515, China.
Xiaojun LuoCancer Center, Traditional Chinese Medicine-Integrated Hospital, Southern Medical University, Guangzhou 510315, China.
Yiyu ChenCancer Research Institute, Southern Medical University, Guangzhou 510515, China.
Xiaojie DengCancer Research Institute, Southern Medical University, Guangzhou 510515, China.
Zixi LiangCancer Research Institute, Southern Medical University, Guangzhou 510515, China.
Xin LiCancer Research Institute, Southern Medical University, Guangzhou 510515, China.
Chao ChengCancer Research Institute, Southern Medical University, Guangzhou 510515, China.
Zhen LiuCancer Research Institute, Southern Medical University, Guangzhou 510515, China.
Weiyi FangCancer Center, Traditional Chinese Medicine-Integrated Hospital, Southern Medical University, Guangzhou 510315, China.
Southern Medical University · CNTCM-Intigrated Cancer Center of Southern Medical University · CNGuangzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The biological role of miR-3188 has not yet been reported in the context of cancer. In this study, we observe that miR-3188 not only reduces cell-cycle transition and proliferation, but also significantly prolongs the survival time of tumour-bearing mice as well as sensitizes cells to 5-FU. Mechanistic analyses indicate that miR-3188 directly targets mTOR to inactivate p-PI3K/p-AKT/c-JUN and induces its own expression. This feedback loop further suppresses cell-cycle signalling through the p-PI3K/p-AKT/p-mTOR pathway. Interestingly, we also observe that miR-3188 direct targeting of mTOR is mediated by FOXO1 suppression of p-PI3K/p-AKT/c-JUN signalling. In clinical samples, reduced miR-3188 is an unfavourable factor and negatively correlates with mTOR and c-JUN levels but positively correlates with FOXO1 expression. Our studies demonstrate that as a tumour suppressor, miR-3188 directly targets mTOR to stimulate its own expression and participates in FOXO1-mediated repression of cell growth, tumorigenesis and NPC chemotherapy resistance.

Indexed as

Gene Expression Regulation, NeoplasticAdultAgedAged, 80 and overAnimalsCarcinomaCell Line, TumorCell Transformation, NeoplasticDrug Resistance, NeoplasmFeedback, PhysiologicalFemaleForkhead Box Protein O1Forkhead Transcription FactorsHumansJNK Mitogen-Activated Protein KinasesMaleForkhead Box Protein O1Forkhead Transcription FactorsFOXO1 protein, humanJNK Mitogen-Activated Protein KinasesMicroRNAsMIRN3189 microRNA, humanMTOR protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine Kinases

Identifiers

PMID27095304
PMCPMC4842991
OpenAlexW2337353755

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.