Evidence map›Paper›PMID 29748795›Full record

ArticleEnvironmental science and pollution research international2018

Role of lncRNAs as prognostic markers of hepatic cancer and potential therapeutic targeting by S-adenosylmethionine via inhibiting PI3K/Akt signaling pathways.

Kadry M Sadek, Mohamed A Lebda, Nasr E Nasr, Sherif M Nasr, Yasser El-Sayed

Abstract read
PubMed Publisher
In one paragraph

Article in Environmental science and pollution research international, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.5field-weighted citation impact, top 20% 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

18 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. IsolatedIranian journal of basic medical sciences · 2024
    Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. 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

5 authors at 3 institutions in 1 country.

Kadry M SadekDepartment of Biochemistry, Faculty of Veterinary Medicine, Damanhour University, Damanhour, Egypt. ksaadek@yahoo.com.ORCID http://orcid.org/0000-0001-8509-6619
Mohamed A LebdaDepartment of Biochemistry, Faculty of Veterinary Medicine, Alexandria University, Alexandria, Egypt.
Nasr E NasrDepartment of Biochemistry, Faculty of Veterinary Medicine, Kafr El-Sheikh University, Kafr El-Sheikh, Egypt.
Sherif M NasrDepartment of Molecular Biology and Genetics, Faculty of Veterinary Medicine, Damanhour University, Damanhour, Egypt.
Yasser El-SayedDepartment of Forensic Medicine and Toxicology, Faculty of Veterinary Medicine, Damanhour University, Damanhour, Egypt.
Damanhour University · EGAlexandria University · EGKafrelsheikh University · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatic cancer (HCC) is a well-identified dilemma throughout the world, and hence, the molecular mechanisms and strategy for preventive protection against this malignancy are critical. S-adenosylmethionine (SAM) is a unique methyl granter in vast reactions, including DNA methylation, and secures the genome against hypomethylation, which is a hallmark of tumors. Consequently, SAM may control the rate of gene expression. The objective of this investigation was to evaluate the expression of long noncoding RNAs (lncRNAs) transcript involved in hepatic tumorigenesis, including additional coding CEBPA (ecCEBPA) and urothelial carcinoma related 1 (UCA1), antioxidant enzymes transcripts, and relevant signaling pathway in diethylnitrosamine (DEN)-prompted HCC along with their conceivable targeting by SAM at different stages of HCC in rats. Our outcomes revealed that SAM particularly when given at the starting phase downregulates ecCEBPA and UCA1 gene transcripts and ameliorate histopathological alterations in DEN-initiated HCC. Interestingly, SAM attenuates DEN-induced upregulation of PI3K/Akt protein expression. However, SAM upregulates the antioxidant enzymes mRNA transcripts and effectively diminishing DNA oxidation. The results of a DNA fragmentation assay further support the capacity of SAM to ameliorate DEN-induced hepatic malignancy. These results revealed the role of ecCEBPA and UCA1 in HCC and suggest that these lncRNAs may be helpful as prognostic and analytical biomarkers of HCC. Curiously, SAM readily targets the studied genes via inhibiting PI3K/Akt signaling pathway, which should make SAM an appealing agent for both chemoprevention and treatment of HCC.

Indexed as

Gene ExpressionAnimalsAntineoplastic AgentsAntioxidantsBase SequenceBiomarkersCarcinoma, HepatocellularCCAAT-Enhancer-Binding ProteinsMalePhosphatidylinositol 3-KinasesPrognosisProtein TransportProto-Oncogene Proteins c-aktRandom AllocationRatsRNA, Long NoncodingAntineoplastic AgentsAntioxidantsBiomarkersCCAAT-Enhancer-Binding ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRNA, Long NoncodingS-AdenosylmethionineDNA oxidationGene expressionHepatic cancerlncRNAsPI3K/Akt pathway

Identifiers

PMID29748795
OpenAlexW2801719693

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.