Evidence map›Paper›PMID 27072512›Full record

ReviewJournal of cellular and molecular medicine2016

Vimentin, colon cancer progression and resistance to butyrate and other HDACis.

Darina L Lazarova, Michael Bordonaro

Open access · goldAbstract readReview
In one paragraph

Review in Journal of cellular and molecular medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
4.2field-weighted citation impact, top 6% 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

38 citing papers in PubMed, 67 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Journal of experimental pharmacology · 2025
    Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Evasion of NK cell immune surveillanceFrontiers in immunology · 2022
    Article
  13. Article
  14. Review
  15. Article
  16. Evaluation ofFood & nutrition research · 2021
    Article
  17. Article
  18. Comparative genomics of the genusMicrobial genomics · 2020
    Article
  19. Article
  20. Article
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.

Darina L LazarovaDepartment of Basic Sciences, The Commonwealth Medical College, Scranton, PA, USA.
Michael BordonaroDepartment of Basic Sciences, The Commonwealth Medical College, Scranton, PA, USA.
Commonwealth Medical College · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dietary fibre protects against colorectal cancer (CRC) most likely through the activity of its fermentation product, butyrate. Butyrate functions as a histone deacetylase inhibitor (HDACi) that hyperactivates Wnt signalling and induces apoptosis of CRC cells. However, individuals who consume a high-fibre diet may still develop CRC; therefore, butyrate resistance may develop over time. Furthermore, CRC cells that are resistant to butyrate are cross-resistant to clinically relevant therapeutic HDACis, suggesting that the development of butyrate resistance in vivo can result in HDACi-resistant CRCs. Butyrate/HDACi-resistant CRC cells differ from their butyrate/HDACi-sensitive counterparts in the expression of many genes, including the gene encoding vimentin (VIM) that is usually expressed in normal mesenchymal cells and is involved in cancer metastasis. Interestingly, vimentin is overexpressed in butyrate/HDACi-resistant CRC cells although Wnt signalling is suppressed in such cells and that VIM is a Wnt activity-targeted gene. The expression of vimentin in colonic neoplastic cells could be correlated with the stage of neoplastic progression. For example, comparative analyses of LT97 microadenoma cells and SW620 colon carcinoma cells revealed that although vimentin is not detectable in LT97 cells, it is highly expressed in SW620 cells. Based upon these observations, we propose that the differential expression of vimentin contributes to the phenotypic differences between butyrate-resistant and butyrate-sensitive CRC cells, as well as to the differences between early-stage and metastatic colorectal neoplastic cells. We discuss the hypothesis that vimentin is a key factor integrating epithelial to mesenchymal transition, colonic neoplastic progression and resistance to HDACis.

Indexed as

Disease ProgressionAnimalsButyric AcidColonic NeoplasmsDrug Resistance, NeoplasmHistone Deacetylase InhibitorsHumansVimentinButyric AcidHistone Deacetylase InhibitorsVimentinbutyratecolorectal cancerepithelial to mesenchymal transitionHDACismicroadenomavimentin

Identifiers

PMID27072512
PMCPMC4882977
OpenAlexW2338323471

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.