Evidence map›Paper›PMID 27446414›Full record

ArticleOncology letters2016

MicroRNA-206 inhibits the viability and migration of human lung adenocarcinoma cells partly by targeting MET.

Xi Chen, Zhong-Kai Tong, Jian-Ya Zhou, Ya-Ke Yao, Shu-Meng Zhang, Jian-Ying Zhou

Open access · diamondAbstract read
In one paragraph

Article in Oncology letters, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

13 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. miR-206/133b Cluster: A Weapon against Lung Cancer?Molecular therapy. Nucleic acids · 2017
    Review
  11. miR-206-3p Inhibits 3T3-L1 Cell Adipogenesis via the c-Met/PI3K/Akt Pathway.International journal of molecular sciences · 2017
    Article
  12. Article
  13. 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

6 authors at 1 institution in 1 country.

Xi ChenDepartment of Respiratory Diseases, Thoracic Disease Diagnosis and Treatment Center, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310003, P.R. China.
Zhong-Kai TongDepartment of Respiratory Diseases, Thoracic Disease Diagnosis and Treatment Center, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310003, P.R. China.
Jian-Ya ZhouDepartment of Respiratory Diseases, Thoracic Disease Diagnosis and Treatment Center, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310003, P.R. China.
Ya-Ke YaoDepartment of Respiratory Diseases, Thoracic Disease Diagnosis and Treatment Center, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310003, P.R. China.
Shu-Meng ZhangDepartment of Respiratory Diseases, Thoracic Disease Diagnosis and Treatment Center, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310003, P.R. China.
Jian-Ying ZhouDepartment of Respiratory Diseases, Thoracic Disease Diagnosis and Treatment Center, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310003, P.R. China.
Zhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNA (miRNA)-based targeting in cancer has emerged as a potential therapeutic strategy. miR-206 has recently been implicated in cancer. However, the role and molecular mechanism of miR-206 in lung adenocarcinoma are still unclear. The present study revealed that miR-206 was downregulated in human lung adenocarcinoma tissues. Overexpression of miR-206 in human lung adenocarcinoma-derived cells significantly inhibited cell viability and migration. Further experiments indicated that the overexpression of miR-206 decreased the expression of MET at the messenger RNA and protein levels via direct targeting of MET in a 3'-untranslated region-dependent manner. The knockdown of MET by small interfering RNA partly led to a phenocopy effect of miR-206. In conclusion, the present study identified miR-206 as a potential tumor suppressor of lung adenocarcinoma that exerts its functions, in part, by negative regulation of MET.

Indexed as

lung cancerMETmiR-206tumor suppressor

Identifiers

PMID27446414
PMCPMC4950289
OpenAlexW2435397387

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.