Evidence map›Paper›PMID 34615998›Full record

ArticleOncogene2022

RANBP1 promotes colorectal cancer progression by regulating pre-miRNA nuclear export via a positive feedback loop with YAP.

Dandan Zheng, Meng Cao, Siyu Zuo, Xin Xia, Chunchun Zhi, Yanbing Lin, Sitong Deng, Xiaoqin Yuan

Erratum issuedAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2022. 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 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

14 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. LncRNAJournal of biomedical research · 2024
    Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. TEAD4 as an Oncogene and a Mitochondrial Modulator.Frontiers in cell and developmental biology · 2022
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 1 country.

Dandan Zheng *Department of Anatomy, Histology and Embryology, Nanjing Medical University, Nanjing, 211166, China.
Meng Cao *Department of General Surgery, Nanjing Drum Tower Hospital, the Affiliated Hospital of Nanjing University Medical School, Nanjing, 210008, China.
Siyu Zuo *Department of Anatomy, Histology and Embryology, Nanjing Medical University, Nanjing, 211166, China.
Xin XiaDepartment of Anatomy, Histology and Embryology, Nanjing Medical University, Nanjing, 211166, China.
Chunchun ZhiDepartment of Pathology, Nanjing Jinling Hospital, Nanjing University School of Medicine, Nanjing, 210002, China.
Yanbing LinDepartment of Anatomy, Histology and Embryology, Nanjing Medical University, Nanjing, 211166, China.
Sitong DengDepartment of Anatomy, Histology and Embryology, Nanjing Medical University, Nanjing, 211166, China.
Xiaoqin YuanDepartment of Anatomy, Histology and Embryology, Nanjing Medical University, Nanjing, 211166, China. yuanxq@njmu.edu.cn.ORCID http://orcid.org/0000-0002-3084-5624
Nanjing Medical University · CNChildren's Hospital of Zhejiang University · CNNanjing Drum Tower Hospital · CNNanjing General Hospital of Nanjing Military Command · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Colorectal cancer (CRC) is among the top five most common malignant tumors worldwide and has a high mortality rate. Identification of the mechanism of CRC and potential therapeutic targets is critical for improving survival. In the present study, we observed high expression of RAN binding protein 1 (RANBP1) in CRC tissues. Upregulated RANBP1 expression was strongly associated with TNM stages and was an independent risk factor for poor prognosis. In vitro and in vivo functional experiments demonstrated that RANBP1 promoted the proliferation and invasion of CRC cells and inhibited the apoptosis of CRC cells. Low RANBP1 expression reduced the expression levels of hsa-miR-18a, hsa-miR-183, and hsa-miR-106 microRNAs (miRNAs) by inhibiting the nucleoplasmic transport of precursor miRNAs (pre-miRNAs), thereby promoting the accumulation of the latter in the nucleus and reducing the expression of mature miRNAs. Further experiments and bioinformatic analyses demonstrated that RANBP1 promoted the expression of YAP by regulating miRNAs and the Hippo pathway. We also found that YAP acted as a transcriptional cofactor to activate RANBP1 transcription in combination with TEAD4 transcription factor. Thus, RANBP1 further promoted the progression of CRC by forming a positive feedback loop with YAP. Our results revealed the biological role and mechanism of RANBP1 in CRC for the first time, suggesting that RANBP1 can be used as a diagnostic molecule and a potential therapeutic target in CRC.

Indexed as

Active Transport, Cell NucleusAdaptor Proteins, Signal TransducingColorectal NeoplasmsDisease ProgressionGene Expression Regulation, NeoplasticMicroRNAsTranscription FactorsYAP-Signaling ProteinsAnimalsApoptosisCell Line, TumorCell NucleusCell ProliferationFeedback, PhysiologicalFemaleHumansAdaptor Proteins, Signal TransducingMicroRNAsNuclear ProteinsPhosphoproteinsran-binding protein 1Transcription FactorsYAP1 protein, humanYAP-Signaling Proteins

Identifiers

PMID34615998
OpenAlexW3204582550

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.