Evidence map›Paper›PMID 15810631›Full record

ArticleDigestive diseases and sciences2005

Butyrate-induced differentiation of colon cancer cells is PKC and JNK dependent.

Arkadiusz Orchel, Zofia Dzierzewicz, Beata Parfiniewicz, Ludmiła Weglarz, Tadeusz Wilczok

Abstract readComparative Study
PubMed Publisher
In one paragraph

Article in Digestive diseases and sciences, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

34 citing papers in PubMed, 95 citations in OpenAlex.

  1. Preventive Effect of Butyrate in Colon Cancer Cell Metabolism.International journal of molecular sciences · 2026
    Article
  2. Mechanisms and Strategies to Overcome Drug Resistance in Colorectal Cancer.International journal of molecular sciences · 2025
    Review
  3. Article
  4. Article
  5. Review
  6. Interdisciplinary insights into the link between gut microbiome and gastric carcinogenesis-what is currently known?Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2022
    Review
  7. Review
  8. Plants (Basel, Switzerland) · 2021
    Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
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  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

5 authors at 1 institution in 1 country.

Arkadiusz OrchelDepartment of Biopharmacy, Medical University of Silesia, 41-200 Sosnowiec, Poland. aorchel@slam.katowice.pl
Zofia Dzierzewicz
Beata Parfiniewicz
Ludmiła Weglarz
Tadeusz Wilczok
Medical University of Silesia · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Butyric acid, a short-chain fatty acid physiologically present in human large gut, is derived from bacterial fermentation of complex carbohydrates. It has been shown to reduce the growth and motility of colon cancer cell lines and to induce cell differentiation and apoptosis. Apoptosis is considered a result of normal colonocyte terminal differentiation in vivo. The aim of this study was to characterize the cellular mechanisms regulating differentiation of colon cancer cells stimulated with sodium butyrate (NaB). The two human colon cancer cell lines Caco-2 and HT-29 were treated with NaB at physiologically relevant concentrations. Alkaline phosphatase (ALP) activity, a marker of colonocyte differentiation, was increased 48 hr after treatment with 1 mM NaB. Higher doses of NaB (5 and 10 mM) induced apoptosis of the cells and failed to stimulate the colonocyte differentiation. Therefore, we assumed that butyrate augments cell differentiation and induces apoptosis, acting via various intracellular mechanisms, and butyrate-mediated programmed cell death cannot be considered a consequence of colonocyte terminal differentiation. The effect of NaB on ALP activity was significantly attenuated in the presence of inhibitors of protein kinase C and JNK. Inhibition of MEK-ERK signal transduction pathways augmented the impact of butyrate on colonocyte differentiation. These results suggest that butyrate could influence the colonocyte differentiation via modulation of the activity of cellular protein kinases and signal transduction.

Indexed as

ApoptosisButyratesCaco-2 CellsCell DifferentiationCell SurvivalColonic NeoplasmsEnzyme ActivationHT29 CellsHumansJNK Mitogen-Activated Protein KinasesProtein Kinase CSensitivity and SpecificitySignal TransductionTumor Cells, CulturedButyratesJNK Mitogen-Activated Protein KinasesProtein Kinase C

Identifiers

PMID15810631
OpenAlexW2078297169

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.