Evidence map›Paper›PMID 22086675›Full record

ArticleMolecular carcinogenesis2013

Effect of silibinin in human colorectal cancer cells: targeting the activation of NF-κB signaling.

Komal Raina, Chapla Agarwal, Rajesh Agarwal

Abstract read
In one paragraph

Article in Molecular carcinogenesis, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
3.5field-weighted citation impact, top 8% 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

41 citing papers in PubMed, 79 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Silymarin and Inflammation: Food for Thoughts.Antioxidants (Basel, Switzerland) · 2024
    Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Silymarin (milk thistle extract) as a therapeutic agent in gastrointestinal cancer.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021
    Review
  16. Article
  17. Review
  18. 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

3 authors at 2 institutions in 1 country.

Komal RainaDepartment of Pharmaceutical Sciences, School of Pharmacy, University of Colorado Denver, Aurora, Colorado 80045, USA.
Chapla Agarwal
Rajesh Agarwal
University of Colorado Denver · USUniversity of Colorado Cancer Center · US

Funding

Colon Cancer Chemoprevention by Flavonoid SilibininR01CA112304 · NCI · UNIVERSITY OF COLORADO DENVER · PI AGARWAL, RAJESH · 2005 to 2015
$2.9M
NCI NIH HHS R01 CA112304
6 · The paper itself

Abstract

Chronic inflammation is one of the primary causes of colorectal cancer (CRC), and major inflammatory pathways implicated in CRC are cyclooxygenase-2 (COX-2) and iNOS; both regulated by nuclear factor-kappa B (NF-κB) suggesting that inhibitors of these pathways could be ideal against CRC. Silibinin has shown promising efficacy against various malignancies including CRC, and therefore here we assessed whether silibinin targets NF-κB activation and associated signaling as a mechanism of its anti-inflammatory and anti-cancer effects in CRC. Our results indicated that silibinin treatment (50-200 µM) of human CRC SW480, LoVo, and HT29 cells strongly inhibits tumor necrosis factor α-induced NF-κB activation together with decreased nuclear levels of both p65 and p50 sub-units. Silibinin also significantly increased IκBα level with a concomitant decrease in phospho-IκBα, without any effect on TNFR1, TRADD, and RIP2, indicating its inhibitory effect on IκB kinase α activity. Next we assessed the effect of oral silibinin feeding on NF-κB pathway in SW480 (COX-2 negative) and LoVo (COX-2 positive) tumor xenografts in nude mice. Together with its inhibitory efficacy on tumor growth and progression, silibinin inhibited NF-κB activation in both xenografts. The protein levels of various NF-κB-regulated molecules such as Bcl-2, COX-2, iNOS, VEGF, and MMPs were also decreased by silibinin in both cell culture studies and xenograft analyses, suggesting its potential to alter NF-κB transcriptional activity. Together, these findings are highly significant in establishing for the first time that silibinin suppresses CRC growth and progression possibly through its anti-inflammatory activity by interfering with NF-κB activation and thus has potential against human CRC.

Indexed as

Administration, OralAnimalsAnti-Inflammatory Agents, Non-SteroidalCell Line, TumorColorectal NeoplasmsDrug Screening Assays, AntitumorHT29 CellsHumansMaleMiceMice, NudeNF-kappa BProtein TransportSignal TransductionSilybinSilymarinAnti-Inflammatory Agents, Non-SteroidalNF-kappa BSilybinSilymarinTumor Necrosis Factor-alpha

Identifiers

PMID22086675
PMCPMC3563833
OpenAlexW2004214213

What OpenQuestion holds

Textmetadata
LicenceTDM
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.