Evidence map›Paper›PMID 26311153›Full record

ArticleMolecular biology reports2015

Anticarcinogenic action of quercetin by downregulation of phosphatidylinositol 3-kinase (PI3K) and protein kinase C (PKC) via induction of p53 in hepatocellular carcinoma (HepG2) cell line.

Akhilendra Kumar Maurya, Manjula Vinayak

Abstract read
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In one paragraph

Article in Molecular biology reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed, 1 pooled it
5.6field-weighted citation impact, top 3% 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

67 citing papers in PubMed, 1 synthesis or guideline pooled it, 132 citations in OpenAlex.

  1. Pooled it
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  3. Article
  4. Review
  5. Review
  6. Review
  7. Neoteric Role of Quercetin in Visual Disorders.Current drug research reviews · 2024
    Review
  8. Article
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  11. Article
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  17. Article
  18. Unravelling Potential Health-Beneficial Properties ofPharmaceuticals (Basel, Switzerland) · 2022
    Review
  19. Article
  20. Therapeutic Applications of the CRISPR-Cas System.Bioengineering (Basel, Switzerland) · 2022
    Review

7 more citing papers are in PubMed but not listed here.

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.

Akhilendra Kumar MauryaBiochemistry & Molecular Biology Laboratory, Centre of Advanced Study in Zoology, Banaras Hindu University, Varanasi, 221005, India, akhilendra28bhu@gmail.com.
Manjula Vinayak
Banaras Hindu University · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Protein kinase C (PKC) is a key regulator of cell growth and differentiation in mammalian cells and hyperactivation of PKC is believed to play an important role in tumor progression. PKC is downstream to signaling protein of phosphatidylinositol 3-Kinase (PI3K), a known up-regulator of cell proliferation and survival. Accumulation of reactive oxygen species (ROS) triggers oxidative stress in the tumor microenvironment, leading to the hyperactivation of various oxidative stress-stimulated signaling molecules. Quercetin (QUE) is a naturally occurring dietary flavonoid having antioxidant properties. QUE is reported to show antitumor activity both in vitro and in vivo; however, the molecular mechanism is yet to be thoroughly explored. HepG2 cells display cellular functions similar to the normal hepatocytes with high degree of morphological and functional differentiation, therefore HepG2 cell line is chosen as the suitable model for drug targeting. Present study is aimed to establish the signaling pathway involved in the anticarcinogenic action of QUE in HepG2 cell line. HepG2 cells were treated with different doses of QUE. Protein level and gene expression were analysed by Western blotting and RT-PCR, respectively. PKC activity was measured by non-radioactive-tagged phosphorylation. Results showed downregulation of expression of PI3K, PKC, COX-2 and ROS caused by QUE. Additionally, QUE enhanced the expression of p53 and BAX in HepG2 cells. Overall, results of the current study suggested that QUE elicited anticarcinogenic action by upregulation of p53 and BAX in HepG2 cells via downregulation of ROS, PKC, PI3K and COX-2, confirming our earlier report on the animal model.

Indexed as

Anticarcinogenic Agentsbcl-2-Associated X ProteinCarcinoma, HepatocellularCyclooxygenase 2Down-RegulationHep G2 CellsHumansLiver NeoplasmsPhosphatidylinositol 3-KinaseProtein Kinase CQuercetinSignal TransductionTumor Suppressor Protein p53Up-RegulationAnticarcinogenic AgentsBAX protein, humanbcl-2-Associated X ProteinCyclooxygenase 2Phosphatidylinositol 3-KinaseProtein Kinase CPTGS2 protein, humanQuercetinTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID26311153
OpenAlexW2210526074

What OpenQuestion holds

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Read underepoch 390

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.