Evidence map›Paper›PMID 31400051›Full record

ArticleJournal of cellular and molecular medicine2019

PON1 hypermethylation is associated with progression of renal cell carcinoma.

Xin Li, Qian Yu

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 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

17 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Plasma proteome fingerprint in kidney diseases.Frontiers in molecular biosciences · 2024
    Article
  10. Article
  11. Review
  12. The Relationship between Cancer and Paraoxonase 1.Antioxidants (Basel, Switzerland) · 2022
    Review
  13. Article
  14. Article
  15. Article
  16. Long Non-coding RNAFrontiers in oncology · 2020
    Article
  17. 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

2 authors at 1 institution in 1 country.

Xin LiDepartment of Pharmacy, China-Japan Union Hospital of Jilin University, Changchun, China.
Qian YuDepartment of Pharmacy, China-Japan Union Hospital of Jilin University, Changchun, China.ORCID 0000-0001-7055-164X
Union Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In this study, our aim was to exploring the influences of DNA methylation of PON1 on cell proliferation, migration and apoptosis of renal cancer cells. The genome-wide methylation array of renal cell carcinoma samples and adjacent tissues were obtained from the cancer genome atlas (TCGA) database. By analysing the DNA methylation and conducting the CpG islands array, methylation status expressed in renal tumour samples and normal renal tissue samples were detected. Methylation-specific PCR (MS-PCR) and qRT-PCR were employed to detect the methylation level and mRNA expression of PON1. Wound-healing assay, transwell assay and MTT assay were utilized to detecting the migration, invasion and proliferation abilities, respectively. The cell apoptosis was testified by Tunnel assay. In addition, the effect of PON1 on renal cancer cells was verified by experiments in vivo. The methylation status of different genes in renal cell carcinoma samples was obtained by CpG islands arrays and hypermethylated PON1 was selected for further study. PON1 was down-regulated in renal cell carcinoma tissues detected by qRT-PCR and Western blot. Both in vitro and vivo experiments indicated that the sunitinib-resistant in renal cancer cells could be suppressed by treat with 5-Aza-dC or TSA, and the effect came out more obvious after 5-Aza-dC and TSA co-treatment. In detail, the demethylation of PON1 inhibited the migration, invasion and proliferation of renal cancer cells and also arrested more cells in G0/G1 phase. The vivo experiment indicated that demethylated PON1 suppressed the growth of tumour. Hypermethylated PON1 promoted migration, invasion and proliferation of sunitinib-resistance renal cancer cells and arrested more cells in G0/G1 phase.

Indexed as

AnimalsAntineoplastic Combined Chemotherapy ProtocolsAryldialkylphosphataseAzacitidineCarcinoma, Renal CellCell Line, TumorCell MovementCell ProliferationCpG IslandsDatabases, GeneticDisease ProgressionDNA MethylationDrug Resistance, NeoplasmEpigenesis, GeneticG1 Phase Cell Cycle CheckpointsGene Expression Regulation, NeoplasticAryldialkylphosphataseAzacitidineHydroxamic AcidsPON1 protein, humanSunitinibtrichostatin A5-Aza-dCDNA methylationPON1renal cell carcinomasunitinibTSA

Identifiers

PMID31400051
PMCPMC6787518
OpenAlexW2967034157

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.