Evidence map›Paper›PMID 24609899›Full record

ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2014

miR-199a-3p inhibits hepatocyte growth factor/c-Met signaling in renal cancer carcinoma.

Jiwei Huang, BaiJun Dong, Jin Zhang, Wen Kong, Yonghui Chen, Wei Xue, Dongming Liu, Yiran Huang

Abstract read
PubMed Publisher
In one paragraph

Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 9% 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, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Crosstalk Mechanisms Between HGF/c-Met Axis and ncRNAs in Malignancy.Frontiers in cell and developmental biology · 2020
    Review
  6. Article
  7. Article
  8. HGF/c-MET: A Promising Therapeutic Target in the Digestive System Cancers.International journal of molecular sciences · 2018
    Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Regulation of MET-mediated proliferation of thyroid carcinoma cells by miR-449b.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Article
  20. Article
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.

Jiwei HuangDepartment of Urology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, 168 Pujian Road, Pudong District, Shanghai, 200127, China.
BaiJun Dong
Jin Zhang
Wen Kong
Yonghui Chen
Wei Xue
Dongming Liu
Yiran Huang
Shanghai Jiao Tong University · CNRenji Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNAs (miRNAs) are a class of small non-coding RNAs that bind protein-coding mRNAs and negatively regulate protein expression by translation repression or mRNA cleavage. Accumulating evidence suggests that miRNAs are involved in cancer development and progression, acting as either tumor suppressors or oncogenes. It has been shown that miR-199a-3p was significantly down-regulated in several types of cancers. However, its role and relevance in renal cell carcinoma (RCC) are still largely unknown. Here, we show that miR-199a-3p is significantly down-regulated in human RCC primary tumors and cell lines compared to their non-tumor counterparts. Moreover, the down-regulation of miR-199a-3p is correlated with the histological grade and TNM (tumor-lymph node-metastasis) stage of RCC. Reintroducing miR-199a-3p in RCC cell lines 769-P and Caki-1 inhibited cell proliferation and caused G1 phase arrest. We found that c-Met was up-regulated in RCC cell lines and its expression could be repressed by miR-199a-3p. Moreover, c-Met was up-regulated in RCC primary tumors and reversely correlated with miR-199a-3p expression in the same paired RCC tissues. Reintroducing miR-199a-3p inhibited c-Met expression and led to attenuated activation of c-Met downstream signaling pathways including STAT3, mTOR and ERK1/2. We found that the concentrations of serum hepatocyte growth factor (HGF), the ligand of c-Met receptor, were significantly elevated in RCC patients compared to healthy persons. In addition, HGF treatment could promote proliferation of RCC cells, and the increased cell proliferation was abrogated by miR-199a-3p. Our findings indicated that miR-199a-3p target HGF/c-Met signaling pathway which is crucial for RCC development and suggest that miR-199a-3p may serve as a potential target miRNA for RCC therapy.

Indexed as

AdultAgedCarcinoma, Renal CellCell Line, TumorCell ProliferationFemaleHepatocyte Growth FactorHumansKidney NeoplasmsMaleMicroRNAsMiddle AgedProto-Oncogene Proteins c-metSignal TransductionHepatocyte Growth FactorMicroRNAsmirn199 microRNA, humanProto-Oncogene Proteins c-met

Identifiers

PMID24609899
OpenAlexW2045756380

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.