Evidence map›Paper›PMID 33318473›Full record

ArticleCell death & disease2020

An autoregulatory feedback loop of miR-21/VMP1 is responsible for the abnormal expression of miR-21 in colorectal cancer cells.

Caixia Wang, Rui Peng, Min Zeng, Zhenhua Zhang, Shengpeng Liu, Dan Jiang, Yuanyuan Lu, Fangdong Zou

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing 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

32 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
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  13. Oncofetal IGF2BP3-mediated control of microRNA structural diversity in the malignancy of early-stage lung adenocarcinoma.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  14. Exploring the Key Signaling Pathways and ncRNAs in Colorectal Cancer.International journal of molecular sciences · 2024
    Review
  15. Review
  16. Article
  17. Article
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  19. Article
  20. The role of miRNAs in Behçet's disease.Frontiers in immunology · 2023
    Review
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

8 authors at 2 institutions in 1 country.

Caixia WangCollege of Life Sciences, Sichuan University, Chengdu, Sichuan, P.R. China.
Rui PengCollege of Life Sciences, Sichuan University, Chengdu, Sichuan, P.R. China.
Min ZengCollege of Life Sciences, Sichuan University, Chengdu, Sichuan, P.R. China.
Zhenhua ZhangCollege of Life Sciences, Sichuan University, Chengdu, Sichuan, P.R. China.
Shengpeng LiuCollege of Life Sciences, Sichuan University, Chengdu, Sichuan, P.R. China.
Dan JiangWest China Hospital of Pathology, Sichuan University, Chengdu, Sichuan, P.R. China.
Yuanyuan LuXijing Hospital of Digestive Disease, Fourth Military Medical University, Xi'an, Shanxi, P.R. China.ORCID 0000-0003-0194-8074
Fangdong ZouCollege of Life Sciences, Sichuan University, Chengdu, Sichuan, P.R. China. fundzou@scu.edu.cn.ORCID 0000-0003-4011-0856
Sichuan University · CNXijing Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MircoRNA-21 (miR-21) was found to be highly expressed in various solid tumors, and its oncogenic properties have been extensively studied in recent years. However, the reason why miR-21 is highly expressed in various tumors remains elusive. Here, we found that the expression of miR-21 was negatively correlated with the expression of vacuole membrane protein-1 (VMP1) in colorectal cancer. Transcription of VMP1 activated either by small activating RNA (saRNA) or transcriptional activator GLI3 inhibited miR-21 expression through reducing its transcripts of VMP1-miR-21 and pri-miR-21, while no significant change in miR-21 expression after exogenous overexpression VMP1 in colorectal cancer cell HCT116. Considering the overlapping location of VMP1 and miR-21 gene in genome, the result suggested that the transcription of miR-21 was inhibited by the endogenous transcriptional activation of VMP1. Furthermore, we identified that miR-21 inhibited the activation and nuclear translocation of transcription factor EB (TFEB) through reducing the inhibitory of PTEN on AKT phosphorylation, which can directly activate the transcription of VMP1. Loss of miR-21 significantly increased VMP1 expression, which could be blocked by PTEN inhibitor (VO-Ohpic) or TFEB siRNA. These results showed that miR-21 negatively regulated VMP1 transcription through the PTEN/AKT/TFEB pathway, and TFEB-induced transcriptional activation of VMP1 could inhibit miR-21 expression, thus forming a feedback regulatory loop of miR-21/VMP1. We further found that disrupting the miR-21/VMP1 feedback loop will decrease the expression of miR-21, reduce the malignancy, and increase their sensitivity to 5-fluorouracil in colorectal cancer cells. Taken together, our results revealed a novel regulatory mechanism of miR-21 expression, and targeting the miR-21/VMP1 feedback loop may provide a new approach to inhibit miR-21 expression in colorectal cancer cells.

Indexed as

Feedback, PhysiologicalGene Expression Regulation, NeoplasticAutophagyBase SequenceBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsCell Line, TumorColorectal NeoplasmsHumansMembrane ProteinsMicroRNAsModels, BiologicalPromoter Regions, GeneticProtein BindingProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseSignal TransductionBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsMembrane ProteinsMicroRNAsMIRN21 microRNA, humanProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseTFEB protein, humanVMP1 protein, human

Identifiers

PMID33318473
PMCPMC7736343
OpenAlexW3113103754

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.