Evidence map›Paper›PMID 25116684›Full record

ArticleInternational journal of molecular sciences2014

Rapamycin-Induced apoptosis in HGF-stimulated lens epithelial cells by AKT/mTOR, ERK and JAK2/STAT3 pathways.

Fang Tian, Lijie Dong, Yu Zhou, Yan Shao, Wenbo Li, Hong Zhang, Fei Wang

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.8field-weighted citation impact, top 10% 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, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Roles of growth factors in eye development and ophthalmic diseases.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2022
    Review
  6. Article
  7. HGF/c-Met: A Key Promoter in Liver Regeneration.Frontiers in pharmacology · 2022
    Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
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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 2 institutions in 1 country.

Fang TianTianjin Medical University Eye Hospital& Eye Institute, No. 251, Fu Kang Road, Nan Kai District, Tianjin 300384, China. tianfang1216@126.com.
Lijie DongTianjin Medical University Eye Hospital& Eye Institute, No. 251, Fu Kang Road, Nan Kai District, Tianjin 300384, China. aitaomubang@126.com.
Yu ZhouTianjin Medical University Eye Hospital& Eye Institute, No. 251, Fu Kang Road, Nan Kai District, Tianjin 300384, China. snail.mutou@163.com.
Yan ShaoTianjin Medical University Eye Hospital& Eye Institute, No. 251, Fu Kang Road, Nan Kai District, Tianjin 300384, China. 13752613234@163.com.
Wenbo LiTianjin Medical University Eye Hospital& Eye Institute, No. 251, Fu Kang Road, Nan Kai District, Tianjin 300384, China. wenboli0412@126.com.
Hong ZhangTianjin Medical University Eye Hospital& Eye Institute, No. 251, Fu Kang Road, Nan Kai District, Tianjin 300384, China. tmuechong@sina.com.
Fei WangTianjin Medical University Eye Hospital& Eye Institute, No. 251, Fu Kang Road, Nan Kai District, Tianjin 300384, China. wangfei@berkgen.com.
Tianjin Medical University · CNTianjin Medical University Eye Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocyte growth factor (HGF) induced the proliferation of lens epithelial cells (LECs) and may be a major cause of posterior capsule opacification (PCO), which is the most frequent postoperative complication of cataract surgery. To date, several agents that can block LECs proliferation have been studied, but none have been used in clinic. Recently, accumulating evidence has suggested rapamycin, the inhibitor of mTOR (mammalian target of Rapamycin), was associated with the induction of apoptosis in LECs. The purpose of our study was to investigate the potential effects of rapamycin on HGF-induced LECs and the underlying mechanisms by which rapamycin exerted its actions. Using cell proliferation, cell viability and flow cytometric apoptosis assays, we found that rapamycin potently not only suppressed proliferation but also induced the apoptosis of LECs in a dose-dependent manner under HGF administration. Further investigation of the underlying mechanism using siRNA transfection revealed that rapamycin could promote apoptosis of LECs via inhibiting HGF-induced phosphorylation of AKT/mTOR, ERK and JAK2/STAT3 signaling molecules. Moreover, the forced expression of AKT, ERK and STAT3 could induce a significant suppression of apoptosis in these cells after treatment of rapamycin. Together, these findings suggested that rapamycin-induced apoptosis in HGF-stimulated LECs is accompanied by inhibition of AKT/mTOR, ERK and JAK2/STAT3 pathways, which supports its use to inhibit PCO in preclinical studies and provides theoretical foundation for future possible practice.

Indexed as

ApoptosisCell ProliferationCells, CulturedEpithelial CellsHepatocyte Growth FactorHumansJanus Kinase 2Lens, CrystallineMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Proto-Oncogene Proteins c-aktSignal TransductionSirolimusSTAT3 Transcription FactorTOR Serine-Threonine KinasesHepatocyte Growth FactorJAK2 protein, humanJanus Kinase 2Mitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3MTOR protein, humanProto-Oncogene Proteins c-aktSirolimusSTAT3 Transcription FactorTOR Serine-Threonine Kinases

Identifiers

PMID25116684
PMCPMC4159827
OpenAlexW2122802536

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.