Evidence map›Paper›PMID 29242604›Full record

ArticleOncogene2018

Ribosomal protein S15a promotes tumor angiogenesis via enhancing Wnt/β-catenin-induced FGF18 expression in hepatocellular carcinoma.

Pengyi Guo, Yi Wang, Chunxiu Dai, Chonglin Tao, Fang Wu, Xiaozai Xie, Haitao Yu, Qiandong Zhu, Junjian Li, Longyun Ye and 6 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

46 citing papers in PubMed, 71 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Research Progress of Ribosomal Proteins in Reproductive Development.International journal of molecular sciences · 2024
    Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. mInternational journal of oncology · 2024
    Article
  14. Article
  15. Article
  16. Ribosome heterogeneity in development and disease.Frontiers in cell and developmental biology · 2024
    Article
  17. Article
  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

16 authors at 3 institutions in 2 countries.

Pengyi GuoDepartment of Hepatobiliary Surgery, The First Affiliated Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Yi WangResearch Center of Evidence-based Medicine and Clinical Epidemiology, School of Public Health and management, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Chunxiu DaiDepartment of Traditional Chinese Medicine, The First Affiliated Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Chonglin TaoDepartment of Hepatobiliary Surgery, The First Affiliated Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Fang WuDepartment of Gastroenterology, The First Affiliated Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Xiaozai XieDepartment of Hepatobiliary Surgery, The First Affiliated Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Haitao YuDepartment of Hepatobiliary Surgery, The First Affiliated Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Qiandong ZhuDepartment of Hepatobiliary Surgery, The First Affiliated Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Junjian LiDepartment of Hepatobiliary Surgery, The First Affiliated Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Longyun YeDepartment of Hepatobiliary Surgery, The First Affiliated Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Fuxiang YuDepartment of Hepatobiliary Surgery, The First Affiliated Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Yunfeng ShanDepartment of Hepatobiliary Surgery, The First Affiliated Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Zhengping YuDepartment of Hepatobiliary Surgery, The First Affiliated Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Renumathy DhanasekaranDivision of Gastroenterology and Hepatology, Stanford University, Palo Alto, CA, USA.
Rongyuan ZhengDepartment of Neurology, The First Affiliated Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, China. zhengry@aliyun.com.
Gang ChenDepartment of Hepatobiliary Surgery, The First Affiliated Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, China. cg_2188@hotmail.com.
First Affiliated Hospital of Wenzhou Medical University · CNWenzhou Medical University · CNStanford University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ribosomal protein s15a (RPS15A) plays a promotive role in the mRNA/ribosome interactions during early translation. Our previous study has found that inhibiting RPS15A expression can decrease proliferation and induce cell cycle arrest in hepatocellular carcinoma (HCC) cell lines. However, the mechanism underlying the involvement of RPS15A in HCC pathogenesis and the clinical significance of RPS15A expression remain unclear. In this study, an evaluation of RPS15A expression in 110 surgically resected HCCs and matched tumor-adjacent normal tissues revealed an overexpression of RPS15A in HCC, which was correlated with worse survival. In addition, tumor tissue with higher RPS15A expression demonstrated a higher microvascular density (MVD). Subsequently, two HCC cell lines, Huh7 (low-level constitutive RPS15A expression) and HepG2 (high RPS15A expression) were used to further evaluate the role of RPS15A in angiogenesis. The co-culture experiment of HCC cells with endothelial cells revealed that the induced overexpression of RPS15A in Huh7 cells increased the angiogenic potential of HUVEC in a paracrine fashion; conversely, knockdown of RPS15A in HepG2 cells showed an opposite effect. Further analysis indicated that RPS15A modulated FGF signaling by enhancing Wnt/beta-catenin-mediated FGF18 expression in HCC cells. FGF18, in turn, through binding to its FGFR3 receptor on endothelial cells, can activate the AKT and ERK pathway and promotes angiogenesis in a tumor microenvironment. Our in vivo experiment further confirmed that inhibition of RPS15A expression in HCC xenografts dramatically hindered tumor growth and inhibited tumor angiogenesis. Together, our findings suggest that RPS15A promotes angiogenesis in HCCs by enhancing Wnt/beta-catenin induced FGF18 expression. The RPS15A/FGF18 pathway may be a rational target for anti-angiogenic therapy of HCC.

Indexed as

AdultAgedAnimalsApoptosisbeta CateninBiomarkers, TumorCarcinoma, HepatocellularCase-Control StudiesCell ProliferationFemaleFibroblast Growth FactorsFollow-Up StudiesGene Expression Regulation, NeoplasticHumansLiver NeoplasmsLymphatic Metastasisbeta CateninBiomarkers, TumorCTNNB1 protein, humanfibroblast growth factor 18Fibroblast Growth FactorsRibosomal ProteinsRPS15A protein, humanWnt1 ProteinWNT1 protein, human

Identifiers

PMID29242604
OpenAlexW2774663121

What OpenQuestion holds

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Registered trials

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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.