Evidence map›Paper›PMID 27186391›Full record

ReviewAmerican journal of cancer research2016

MicroRNA-338-3p suppresses metastasis of lung cancer cells by targeting the EMT regulator Sox4.

Yang Li, Peirui Chen, Lingling Zu, Bin Liu, Min Wang, Qinghua Zhou

Erratum issuedOpen access · greenAbstract readReview
In one paragraph

Review in American journal of cancer research, 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 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

52 citing papers in PubMed, 70 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Non-coding RNAs as potential biomarkers of gallbladder cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    Review
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  15. Review
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  17. MiR-338-3p improved lung adenocarcinoma byArchives of medical science : AMS · 2021
    Article
  18. Article
  19. PeerJ · 2021
    Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Yang LiTianjin Key Laboratory of Lung Cancer Metastasis and Tumor Microenvironment, Tianjin Lung Cancer Institute, Tianjin Medical University General Hospital Tianjin 300052, China.
Peirui ChenTianjin Key Laboratory of Lung Cancer Metastasis and Tumor Microenvironment, Tianjin Lung Cancer Institute, Tianjin Medical University General Hospital Tianjin 300052, China.
Lingling ZuTianjin Key Laboratory of Lung Cancer Metastasis and Tumor Microenvironment, Tianjin Lung Cancer Institute, Tianjin Medical University General Hospital Tianjin 300052, China.
Bin LiuTianjin Key Laboratory of Lung Cancer Metastasis and Tumor Microenvironment, Tianjin Lung Cancer Institute, Tianjin Medical University General Hospital Tianjin 300052, China.
Min WangTianjin Key Laboratory of Lung Cancer Metastasis and Tumor Microenvironment, Tianjin Lung Cancer Institute, Tianjin Medical University General Hospital Tianjin 300052, China.
Qinghua ZhouTianjin Key Laboratory of Lung Cancer Metastasis and Tumor Microenvironment, Tianjin Lung Cancer Institute, Tianjin Medical University General Hospital Tianjin 300052, China.
Tianjin Medical University Cancer Institute and Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metastasis remains the leading cause of the majority of cancer-related mortality. MicroRNAs (miRNAs) have frequently emerged as tumor metastatic regulator by acting on multiple signaling pathways. In the present study, we demonstrated that miR-338-3p was significantly downregulated in highly metastatic NSCLC cell lines and clinical metastatic tissues. Then, we found that introduction of miR-338-3p significantly suppressed the migration and invasion of lung cancer cells both in vitro and in vivo, suggesting that miR-338-3p may be a novel tumor suppressor. Further studies indicated that the EMT-related transcription factor Sox4 was one direct target gene of miR-338-3p, evidenced by the direct binding of miR-338-3p with the 3'untranslated region (3'UTR) of Sox4. Furthermore, miR-338-3p could decrease the expression of Sox4 both at mRNA and protein levels. Notably, the EMT marker E-cadherin or vimentin, a downstream regulator of Sox4, was also down-regulated or up-regulated upon miR-338-3p treatment. Additionally, over-expressing or silencing Sox4 could elevate or inhibit the migration and invasion of lung cancer cells, parallel to the effect of miR-338-3p on the lung cancer cells. Meanwhile, knockdown of Sox4 reversed the enhanced migration and invasion mediated by miR-338-3p. These results indicated that miR-338-3p suppressed the migration and invasion of NSCLC cells through targeting Sox4 involving in the EMT process. Thus, our finding provides new insight into the mechanism of NSCLC progression. Therapeutically, miR-338-3p may serve as a potential target in the treatment of human lung cancer.

Indexed as

metastasisMiR-338-3pNSCLCsox4

Identifiers

PMID27186391
PMCPMC4859648
OpenAlexW2403305259

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.