Evidence map›Paper›PMID 24788349›Full record

ArticlePloS one2014

Melittin restores PTEN expression by down-regulating HDAC2 in human hepatocelluar carcinoma HepG2 cells.

Hui Zhang, Bin Zhao, Cheng Huang, Xiao-Ming Meng, Er-Bao Bian, Jun Li

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

23 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
  2. Review
  3. Interaction of NF-κB and FOSL1 drives glioma stemness.Cellular and molecular life sciences : CMLS · 2024
    Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. HDAC2 as a target for developing anti-cancer drugs.Computational and structural biotechnology journal · 2023
    Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
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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

6 authors at 1 institution in 1 country.

Hui ZhangSchool of pharmacy, Anhui key laboratory of bioactivity of natural products, Anhui Medical University, Hefei, Anhui Province, China; Institute for Liver Diseases of Anhui Medical University (AMU), Hefei, Anhui Province, China.
Bin ZhaoSchool of pharmacy, Anhui key laboratory of bioactivity of natural products, Anhui Medical University, Hefei, Anhui Province, China; Institute for Liver Diseases of Anhui Medical University (AMU), Hefei, Anhui Province, China.
Cheng HuangSchool of pharmacy, Anhui key laboratory of bioactivity of natural products, Anhui Medical University, Hefei, Anhui Province, China; Institute for Liver Diseases of Anhui Medical University (AMU), Hefei, Anhui Province, China.
Xiao-Ming MengSchool of pharmacy, Anhui key laboratory of bioactivity of natural products, Anhui Medical University, Hefei, Anhui Province, China; Institute for Liver Diseases of Anhui Medical University (AMU), Hefei, Anhui Province, China.
Er-Bao BianSchool of pharmacy, Anhui key laboratory of bioactivity of natural products, Anhui Medical University, Hefei, Anhui Province, China; Institute for Liver Diseases of Anhui Medical University (AMU), Hefei, Anhui Province, China.
Jun LiSchool of pharmacy, Anhui key laboratory of bioactivity of natural products, Anhui Medical University, Hefei, Anhui Province, China; Institute for Liver Diseases of Anhui Medical University (AMU), Hefei, Anhui Province, China.
Anhui Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Melittin is a water-soluble toxic peptide derived from the venom of the bee. Although many studies show the anti-tumor activity of melittin in human cancer including glioma cells, the underlying mechanisms remain elusive. Here the effect of melittin on human hepatocelluar carcinoma HepG2 cell proliferation in vitro and further mechanisms was investigated. We found melittin could inhibit cell proliferation in vitro using Flow cytometry and MTT method. Besides, we discovered that melittin significantly downregulated the expressions of CyclinD1 and CDK4. Results of western Blot and Real-time PCR analysis indicated that melittin was capable to upregulate the expression of PTEN and attenuate histone deacetylase 2 (HDAC2) expression. Further studies demonstrated that knockdown of HDAC2 completely mimicked the effects of melittin on PTEN gene expression. Conversely, it was that the potential utility of melittin on PTEN expression was reversed in cells treated with a recombinant pEGFP-C2-HDAC2 plasmid. In addition, treatment with melittin caused a downregulation of Akt phosphorylation, while overexpression of HDAC2 promoted Akt phosphorylation. These findings suggested that the inhibitory of cell growth by melittin might be led by HDAC2-mediated PTEN upregulation, Akt inactivation, and inhibition of the PI3K/Akt signaling pathways.

Indexed as

Carcinoma, HepatocellularCell Cycle CheckpointsCell ProliferationDown-RegulationHep G2 CellsHistone Deacetylase 2HumansLiver NeoplasmsMelittenProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseSignal TransductionTumor Suppressor ProteinsHistone Deacetylase 2MelittenProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, humanTumor Suppressor Proteins

Identifiers

PMID24788349
PMCPMC4008415
OpenAlexW2073018532

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.