Evidence map›Paper›PMID 26191164›Full record

ArticleInternational journal of clinical and experimental pathology2015

MicroRNA-126 is down-regulated in human esophageal squamous cell carcinoma and inhibits the proliferation and migration in EC109 cell via PI3K/AKT signaling pathway.

Zheng-Chao Nie, Wen-Hao Weng, Yu-Shan Shang, Yin Long, Jing Li, Yan-Ting Xu, Zhi Li

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

19 citing papers in PubMed, 35 citations in OpenAlex.

  1. miR-126: a bridge between cancer and exercise.Cancer cell international · 2025
    Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. 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

7 authors at 3 institutions in 1 country.

Zheng-Chao NieDepartment of Clinical Laboratory, Shanghai Tenth People's Hospital Tongji University, Shanghai 200072, China.
Wen-Hao WengDepartment of Clinical Laboratory, Shanghai Tenth People's Hospital Tongji University, Shanghai 200072, China.
Yu-Shan ShangDepartment of Clinical Laboratory, Chuzhou Second People's Hospital Chuzhou, China.
Yin LongDepartment of Clinical Laboratory, Yangpu Hospital, Tongji University Shanghai 200090, China.
Jing LiDepartment of Clinical Laboratory, Shanghai Tenth People's Hospital Tongji University, Shanghai 200072, China.
Yan-Ting XuDepartment of Clinical Laboratory, Shanghai Tenth People's Hospital Tongji University, Shanghai 200072, China.
Zhi LiDepartment of Clinical Laboratory, Yangpu Hospital, Tongji University Shanghai 200090, China.
Shanghai Tenth People's Hospital · CNYangpu Hospital of Tongji University · CNTaizhou Second People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNA-126 (miR-126) was found down-regulated in different types of cancer including esophageal squamous cell carcinoma (ESCC). However, the onco-genetic role of miR-126 in ESCC still remains unknown. In the present study, we found the relative expression of miR-126 in ESCC was significant decreased in ESCC tissues compared to adjacent normal tissues. Overexpression of miR-126 in EC109 cells resulted in significant decrease in cell proliferation, colon formation and migration. PI3K regulatory subunit p85 beta (PIK3R2), a member of PI3K/AKT signaling pathway was found upregulated in ESCC tissues and there is a negative relation between expression of PIK3R2 and miR-126. Restoration of miR-126 in EC109 cells induced a reduction in PIK3R2 protein levels, accompanied with a substantial reduction in phosphorylated AKT levels in EC109 cells, suggesting impairment in PI3K/AKT signaling pathway. The luciferase reporter assay confirmed that PIK3R2 was a direct target of miR-126. Furthermore, we also indicated overexpression of miR-126 suppresses G2/M transition in EC109 cells. Taken together, our study suggests that miR-126 functions as a potential tumor suppressor in ESCC progression via regulating PI3K/AKT signaling pathway partly by targeting PIK3R2, and targeting of miR-126 may provide a novel strategy for the diagnosis and treatment of ESCC.

Indexed as

Carcinoma, Squamous CellCell CycleCell Line, TumorCell MovementCell ProliferationDisease ProgressionDown-RegulationEsophageal NeoplasmsHumansMicroRNAsPhosphatidylinositol 3-KinasesPhosphorylationProto-Oncogene Proteins c-aktSignal TransductionMicroRNAsMIRN126 microRNA, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktAKTcell cycle arrestESCCmiR-126PIK3R2

Identifiers

PMID26191164
PMCPMC4503036
OpenAlexW975555805

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.