Evidence map›Paper›PMID 25157104›Full record

ArticleThe Journal of biological chemistry2014

Nuclear matrix protein SMAR1 represses c-Fos-mediated HPV18 E6 transcription through alteration of chromatin histone deacetylation.

Samik Chakraborty, Kaushik Das, Shilpi Saha, Minakshi Mazumdar, Argha Manna, Sreeparna Chakraborty, Shravanti Mukherjee, Poulami Khan, Arghya Adhikary, Suchismita Mohanty and 4 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.2field-weighted citation impact, top 9% 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

16 citing papers in PubMed, 32 citations in OpenAlex.

  1. Advances in cervical cancer: current insights and future directions.Cancer communications (London, England) · 2025
    Review
  2. Review
  3. Review
  4. Review
  5. Dietary supplements for treatment of endometriosis: A review.Acta bio-medica : Atenei Parmensis · 2022
    Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Vorinostat, a pan-HDAC inhibitor, abrogates productive HPV-18 DNA amplification.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  11. Morphoproteomics, E6/E7 in-situ hybridization, and biomedical analytics define the etiopathogenesis of HPV-associated oropharyngeal carcinoma and provide targeted therapeutic options.Journal of otolaryngology - head & neck surgery = Le Journal d'oto-rhino-laryngologie et de chirurgie cervico-faciale · 2017
    Article
  12. Article
  13. Article
  14. Histone and Non-Histone Targets of Dietary Deacetylase Inhibitors.Current topics in medicinal chemistry · 2016
    Review
  15. Article
  16. 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

14 authors at 2 institutions in 1 country.

Samik ChakrabortyFrom the Division of Molecular Medicine, Bose Institute, P1/12, Calcutta Improvement Trust Scheme VIIM, Kolkata 700054, West Bengal, India.
Kaushik DasFrom the Division of Molecular Medicine, Bose Institute, P1/12, Calcutta Improvement Trust Scheme VIIM, Kolkata 700054, West Bengal, India.
Shilpi SahaFrom the Division of Molecular Medicine, Bose Institute, P1/12, Calcutta Improvement Trust Scheme VIIM, Kolkata 700054, West Bengal, India.
Minakshi MazumdarFrom the Division of Molecular Medicine, Bose Institute, P1/12, Calcutta Improvement Trust Scheme VIIM, Kolkata 700054, West Bengal, India.
Argha MannaFrom the Division of Molecular Medicine, Bose Institute, P1/12, Calcutta Improvement Trust Scheme VIIM, Kolkata 700054, West Bengal, India.
Sreeparna ChakrabortyFrom the Division of Molecular Medicine, Bose Institute, P1/12, Calcutta Improvement Trust Scheme VIIM, Kolkata 700054, West Bengal, India.
Shravanti MukherjeeFrom the Division of Molecular Medicine, Bose Institute, P1/12, Calcutta Improvement Trust Scheme VIIM, Kolkata 700054, West Bengal, India.
Poulami KhanFrom the Division of Molecular Medicine, Bose Institute, P1/12, Calcutta Improvement Trust Scheme VIIM, Kolkata 700054, West Bengal, India.
Arghya AdhikaryFrom the Division of Molecular Medicine, Bose Institute, P1/12, Calcutta Improvement Trust Scheme VIIM, Kolkata 700054, West Bengal, India.
Suchismita MohantyFrom the Division of Molecular Medicine, Bose Institute, P1/12, Calcutta Improvement Trust Scheme VIIM, Kolkata 700054, West Bengal, India.
Samit Chattopadhyaythe National Centre for Cell Science, Pune University Campus, Ganeshkhind, Pune 411007, Maharashtra, India, and.
Subhash C Biswasthe Department of Gynecology & Obstetrics, Institute of Post-Graduate Medical Education and Research (IPGMER), Seth Sukhlal Karnani Memorial (SSKM) Hospital, Kolkata 700020, West Bengal, India.
Gaurisankar SaFrom the Division of Molecular Medicine, Bose Institute, P1/12, Calcutta Improvement Trust Scheme VIIM, Kolkata 700054, West Bengal, India.
Tanya DasFrom the Division of Molecular Medicine, Bose Institute, P1/12, Calcutta Improvement Trust Scheme VIIM, Kolkata 700054, West Bengal, India, tanya@jcbose.ac.in.
Bose Institute · INSavitribai Phule Pune University · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Matrix attachment region (MAR)-binding proteins have been implicated in the transcriptional regulation of host as well as viral genes, but their precise role in HPV-infected cervical cancer remains unclear. Here we show that HPV18 promoter contains consensus MAR element in the LCR and E6 sequences where SMAR1 binds and reinforces HPV18 E6 transcriptional silencing. In fact, curcumin-induced up-regulation of SMAR1 ensures recruitment of SMAR1-HDAC1 repressor complex at the LCR and E6 MAR sequences, thereby decreasing histone acetylation at H3K9 and H3K18, leading to reorientation of the chromatin. As a consequence, c-Fos binding at the putative AP-1 sites on E6 promoter is inhibited. E6 depletion interrupts degradation of E6-mediated p53 and lysine acetyl transferase, Tip60. Tip60, in turn, acetylates p53, thereby restoring p53-mediated transactivation of proapoptotic genes to ensure apoptosis. This hitherto unexplained function of SMAR1 signifies the potential of this unique scaffold matrix-associated region-binding protein as a critical regulator of E6-mediated anti-apoptotic network in HPV18-infected cervical adenocarcinoma. These results also justify the candidature of curcumin for the treatment of HPV18-infected cervical carcinoma.

Indexed as

Gene Expression Regulation, ViralTranscription, GeneticAcetylationApoptosisCell Cycle ProteinsChromatinDNA-Binding ProteinsHeLa CellsHistonesHumansNuclear ProteinsOncogene Proteins, ViralPromoter Regions, GeneticProtein BindingProto-Oncogene Proteins c-fosTranscription Factor AP-1BANP protein, humanCell Cycle ProteinsChromatinDNA-Binding ProteinsE6 protein, Human papillomavirus type 18HistonesNuclear ProteinsOncogene Proteins, ViralProto-Oncogene Proteins c-fosTranscription Factor AP-1Cancer PreventionFBJ Murine Osteosarcoma Viral Oncogene Homolog (Fos)Histone Deacetylase (HDAC)PapillomavirusTranscription Repressor

Identifiers

PMID25157104
PMCPMC4200262
OpenAlexW1967600468

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.