Evidence map›Paper›PMID 23792459›Full record

ArticleThe Journal of investigative dermatology2014

A signal transduction pathway from TGF-β1 to SKP2 via Akt1 and c-Myc and its correlation with progression in human melanoma.

Xuan Qu, Liangliang Shen, Yan Zheng, Yang Cui, Zhihui Feng, Feng Liu, Jiankang Liu

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in The Journal of investigative dermatology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

31 citing papers in PubMed, 48 citations in OpenAlex.

  1. Review
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  3. Article
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  5. Article
  6. TGF-β1-induced RAP2 regulates invasion in pancreatic cancer.Acta biochimica et biophysica Sinica · 2022
    Article
  7. Article
  8. Review
  9. Review
  10. Alterations in TGFβ signaling during prostate cancer progression.American journal of clinical and experimental urology · 2021
    Review
  11. Article
  12. Article
  13. NDRG2 ablation reprograms metastatic cancer cells towards glutamine dependenceInternational journal of biological sciences · 2020
    Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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 4 institutions in 2 countries.

Xuan QuInstitute of Mitochondrial Biology and Medicine, The Key Laboratory of Biomedical Information Engineering of Ministry of Education, Xi'an Jiaotong University School of Life Science and Technology, Xi'an, China.
Liangliang ShenDepartment of Biochemistry and Molecular Biology, The State Key Laboratory of Cancer Biology, The Fourth Military Medical University, Xi'an, China.
Yan ZhengDepartment of Dermatology, The Second Affiliated Hospital, Xi'an Jiaotong University, Xi'an, China.
Yang CuiInstitute of Mitochondrial Biology and Medicine, The Key Laboratory of Biomedical Information Engineering of Ministry of Education, Xi'an Jiaotong University School of Life Science and Technology, Xi'an, China.
Zhihui FengCenter for Mitochondrial Biology and Medicine, Frontier Institute of Science and Technology, Xi'an Jiaotong University, Xi'an, China. Electronic address: zenyan66@126.com.
Feng LiuDepartment of Medicine, University of California Irvine Medical School, Irvine, California, USA; Chao Family Comprehensive Cancer Center, University of California Irvine Medical School, Irvine, California, USA. Electronic address: liufe@uci.edu.
Jiankang LiuInstitute of Mitochondrial Biology and Medicine, The Key Laboratory of Biomedical Information Engineering of Ministry of Education, Xi'an Jiaotong University School of Life Science and Technology, Xi'an, China.
Xi'an Jiaotong University · CNAir Force Medical University · CNSecond Affiliated Hospital of Xi'an Jiaotong University · CNUniversity of California, Irvine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Both SKP2 (S-phase kinase-associated protein 2) and transforming growth factor-β1 (TGF-β1) play important roles in cancer metastasis through different mechanisms: TGF-β1 via induction of epithelial-mesenchymal transition (EMT) and SKP2 via downregulating p27(kip1). Recent studies indicated that c-Myc and Akt1 were active players in metastasis. In this study we demonstrated a crosstalk between these pathways. Specifically, we found that TGF-β1 treatment increased SKP2 expression accompanied with increased phosphorylation of Akt1 and c-Myc protein accumulation during EMT. We demonstrated that Akt1 was required for TGF-β1-mediated SKP2 upregulation and that c-Myc transcription factor specifically bound to the promoter of SKP2 for its enhanced transcription. Analysis of 25 samples of normal human skin, nevi, and melanomas revealed a positive correlation between c-Myc and SKP2 accumulation. Furthermore, accumulation of SKP2 and c-Myc proteins was significantly higher in metastatic melanoma samples as compared with that in primary melanomas, which again was higher than that in normal skin or nevi. In summary, our results integrated TGF-β1 signals to SKP2 via Akt1 and c-Myc during EMT, and provided, to our knowledge, a previously unreported mechanistic molecular event for TGF-β1-induced metastasis in human melanoma.

Indexed as

Cell Line, TumorDisease ProgressionEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansMelanomaPromoter Regions, GeneticProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-mycSignal TransductionSkin NeoplasmsS-Phase Kinase-Associated ProteinsTranscription, GeneticTransforming Growth Factor beta1AKT1 protein, humanMYC protein, humanProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-mycS-Phase Kinase-Associated ProteinsTransforming Growth Factor beta1

Identifiers

PMID23792459
OpenAlexW2055650359

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.