Evidence map›Paper›PMID 30661291›Full record

ArticleJournal of cellular and molecular medicine2019

RPS15A promotes gastric cancer progression via activation of the Akt/IKK-β/NF-κB signalling pathway.

Chenchen Liu, Xigan He, Xiaowen Liu, Jian Yu, Meng Zhang, Fudong Yu, Yanong Wang

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

29 citing papers in PubMed, 49 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  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 3 institutions in 1 country.

Chenchen LiuDepartment of Gastric Surgery, Fudan University Shanghai Cancer Center, Shanghai, China.
Xigan HeDepartment of Oncology, Shanghai Medical College, Fudan University, Shanghai, China.
Xiaowen LiuDepartment of Gastric Surgery, Fudan University Shanghai Cancer Center, Shanghai, China.
Jian YuDepartment of Oncology, Rizhao Central Hospital, Rizhao, Shandong, China.
Meng ZhangDepartment of Oncology, Shanghai Medical College, Fudan University, Shanghai, China.
Fudong YuKey Laboratory of Reproduction Regulation of NPFPC, SIPPR, IRD, Fudan University, Shanghai, China.
Yanong WangDepartment of Gastric Surgery, Fudan University Shanghai Cancer Center, Shanghai, China.ORCID 0000-0001-8454-2701
Shanghai Medical College of Fudan University · CNFudan University · CNPeople’s Hospital of Rizhao · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study aimed to investigate the clinical significance, potential biological function and underlying mechanism of RPS15A in gastric cancer (GC) progression. RPS15A expression was detected in 40 pairs of GC tissues and matched normal gastric mucosae (MNGM) using qRT-PCR analysis. Immunohistochemistry assay was conducted using a tissue microarray including 186 primary GC samples to characterize the clinical significance of RPS15A. A series of in vitro and in vivo assays were performed to elucidate the biological function of RPS15A in GC development and underlying molecular mechanisms. The expression of RPS15A was significantly up-regulated in GC samples compared to MNGM, and its expression was closely related to TNM stage, tumour size, differentiation, lymph node metastasis and poor patient survival. Ectopic expression of RPS15A markedly enhanced the proliferation and metastasis of GC cells both in vitro and in vivo. RPS15A overexpression also promoted the epithelial-mesenchymal transition (EMT) phenotype formation of GC cells. Investigations of underlying mechanisms found that RPS15A activated the NF-κB signalling pathway by inducing the nuclear translocation and phosphorylation of the p65 NF-κB subunit, transactivation of NF-κB reporter and up-regulating target genes of this pathway. In addition, RPS15A overexpression activated, while RPS15A knockdown inhibited the Akt/IKK-β signalling axis in GC cells. And both Akt inhibitor LY294002 and IKK inhibitor Bay117082 neutralized the p65 and p-p65 nuclear translocation induced by RPS15A overexpression. Collectively, our findings suggest that RPS15A activates the NF-κB pathway through Akt/IKK-β signalling axis, and consequently promotes EMT and GC metastasis. This newly identified RPS15A/Akt/IKK-β/NF-κB signalling pathway may be a potential therapeutic target to prevent GC progression.

Indexed as

AnimalsCell Line, TumorCell ProliferationDisease ProgressionEpithelial-Mesenchymal TransitionFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHumansI-kappa B KinaseKaplan-Meier EstimateMaleMice, NudeMiddle AgedNF-kappa BProto-Oncogene Proteins c-aktI-kappa B KinaseNF-kappa BProto-Oncogene Proteins c-aktRibosomal ProteinsRPS15A protein, humanEpithelial-mesenchymal transitionGastric cancerMetastasisNF-κBRibosomal protein S15A

Identifiers

PMID30661291
PMCPMC6378197
OpenAlexW2910942482

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.