Evidence map›Paper›PMID 32974832›Full record

ArticleMolecular and cellular biochemistry2021

Tumor suppressor genes are differentially regulated with dietary folate modulations in a rat model of hepatocellular carcinoma.

Renuka Sharma, Taqveema Ali, Jyotdeep Kaur

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In one paragraph

Article in Molecular and cellular biochemistry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 45% of its field
1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed, 4 citations in OpenAlex.

  1. Review
4 · The record

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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

3 authors at 1 institution in 1 country.

Renuka SharmaDepartment of Biochemistry, Post Graduate Institute of Medical Education and Research, Chandigarh, India.
Taqveema AliDepartment of Biochemistry, Post Graduate Institute of Medical Education and Research, Chandigarh, India.
Jyotdeep KaurDepartment of Biochemistry, Post Graduate Institute of Medical Education and Research, Chandigarh, India. jyotdeep2001@yahoo.co.in.ORCID http://orcid.org/0000-0003-0284-4517
Post Graduate Institute of Medical Education and Research · IN

Funding

Indian Council of Medical Research JRF/2013/10851
6 · The paper itself

Abstract

The current study evaluated the outcome of dietary folate modulations on the expression of tumor suppressor genes (TSGs) during developmental stages of hepatocellular carcinoma (HCC) in a Wistar rat model. In addition to dietary folate modulations, male rats were administered diethylnitrosamine (DEN) intraperitoneally once a week upto 18 weeks to induce HCC. Serum folate levels were found to be decreased and increased in folate deficiency (FD) and folate-oversupplemented (FO) groups respectively when compared to folate normal (FN) rats. Apoptosis was observed in FD in fibrosis and HCC stages. mRNA expression analysis by RT-PCR of TSGs (DPT, p16, RUNX3, RASSF1A and SOCS1) and protein expression by western blot (RASSF1A, RUNX3 and p16) depicted differential expression in FD and FO in various stages of HCC development. Bisulfite sequencing for p16 and RASSF1A promoter was performed. The promoter region of p16 gene was hypermethylated at 7th and that of RASSF1A was hypomethylated at 10th CpG in cirrhotic category in FD rats. Hyper and hypomethylation at 10th and 24th CpG respectively in RASSF1A promoter was observed in HCC category in both FD and FO groups. All TSGs showed differential expression at transcript and protein level. Increased expression of DPT, RASSF1A, SOCS1 and decreased expression of RUNX3 could be playing role in HCC development in FD rats. Reduced expression of RUNX3, RASSF1A and SOCS1 in HCC category was demonstrated in FO rats. Thus, the studied TSGs are differentially expressed with dietary folate modulations during the development of HCC in DEN-treated rat model and the promoter methylation might be a contributing mechanism under these conditions.

Indexed as

DietGene Expression Regulation, NeoplasticGenes, Tumor SuppressorAnimal FeedAnimalsApoptosisCarcinoma, HepatocellularCore Binding Factor Alpha 3 SubunitDisease Models, AnimalDNA FragmentationDNA MethylationFolic AcidLiver NeoplasmsMaleRatsRats, WistarCore Binding Factor Alpha 3 SubunitFolic AcidRASSF1 protein, ratSocs1 protein, ratSuppressor of Cytokine Signaling 1 ProteinTumor Suppressor ProteinsFolate deficiencyFolate oversupplementationFolic acidHCC

Identifiers

PMID32974832
OpenAlexW3087779058

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.