Evidence map›Paper›PMID 28521431›Full record

ArticleOncology letters2017

MicroRNA-320a is downregulated in non-small cell lung cancer and suppresses tumor cell growth and invasion by directly targeting insulin-like growth factor 1 receptor.

Jianguo Wang, Chunyun Shi, Jianfei Wang, Li Cao, Li Zhong, Dongmei Wang

Open access · diamondAbstract read
In one paragraph

Article in Oncology letters, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

25 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. The Effect of MiR320a on Lung Cancer.MicroRNA (Shariqah, United Arab Emirates) · 2024
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. 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

6 authors at 3 institutions in 1 country.

Jianguo WangCollege of Life Sciences, Agricultural University of Hebei, Baoding, Hebei 071001, P.R. China.
Chunyun ShiDepartment of Pediatrics, Baoding Children's Hospital, Hebei 071000, P.R. China.
Jianfei WangCollege of Life Sciences, Hebei University, Baoding, Hebei 071000, P.R. China.
Li CaoCollege of Life Sciences, Hebei University, Baoding, Hebei 071000, P.R. China.
Li ZhongCollege of Life Sciences, Hebei University, Baoding, Hebei 071000, P.R. China.
Dongmei WangCollege of Life Sciences, Agricultural University of Hebei, Baoding, Hebei 071001, P.R. China.
Hebei University · CNHebei Agricultural University · CNBaoding People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Accumulating evidence has demonstrated that microRNAs (miRs/miRNAs) are implicated in carcinogenesis and cancer progression, and can function as oncogenes or tumor suppressor genes in human cancer types. Previous profile studies of miRNA expression levels have revealed that miR-320a was downregulated in breast cancer, colon cancer, bladder cancer, glioblastoma and salivary adenoid cystic carcinoma. However, its expression level, potential functions and the mechanisms underlying its functions in non-small cell lung cancer (NSCLC) require further investigation. The present study investigated the expression level, biological roles and underlying molecular mechanisms of miR-320a in NSCLC. The expression levels of miR-320a in NSCLC tissue and cell lines were detected using the reverse transcription-quantitative polymerase chain reaction. Cell proliferation and Transwell invasion assays were performed to examine the effects of miR-320a on NSCLC cells. In addition, bioinformatic analysis, western blot analysis and luciferase reporter assays were performed to identify the direct gene target of miR-320a in NSCLC. In the present study it was demonstrated that miR-320a was significantly downregulated in NSCLC tissues and cell lines. Ectopic overexpression of miR-320a suppressed the proliferation and invasion of NSCLC cells. Further studies indicated that miR-320a directly targeted the 3'-untranslated region of insulin-like growth factor 1 receptor (IGF-1R) and suppressed its expression at the mRNA and protein levels. As well as restoring the miR-320a expression level, the knockdown of IGF-1R also decreased the growth and invasion of the NSCLC cells. These results suggested that miR-320a served as a tumor suppressor in the NSCLC cells by directly targeting IGF-1R. Therefore, miR-320a should be investigated as a therapeutic target for the treatment of NSCLC.

Indexed as

growthinsulin-like growth factor 1 receptorinvasionmicroRNA-320anon-small cell lung cancer

Identifiers

PMID28521431
PMCPMC5431336
OpenAlexW2599204909

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.