Evidence map›Paper›PMID 31734898›Full record

ArticleMolecular biology reports2020

Induction of growth cessation by acacetin via β-catenin pathway and apoptosis by apoptosis inducing factor activation in colorectal carcinoma cells.

Nupoor Prasad, Jiten R Sharma, Umesh C S Yadav

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular biology reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

18 citing papers in PubMed, 61 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Effect of acacetin on inhibition of apoptosis inWorld journal of gastrointestinal oncology · 2024
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. 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 1 institution in 1 country.

Nupoor PrasadMetabolic Disorder & Inflammatory Pathologies Laboratory, School of Life Sciences, Central University of Gujarat, Sector -30, Gandhinagar, 382030, Gujarat, India.
Jiten R SharmaMetabolic Disorder & Inflammatory Pathologies Laboratory, School of Life Sciences, Central University of Gujarat, Sector -30, Gandhinagar, 382030, Gujarat, India.
Umesh C S YadavMetabolic Disorder & Inflammatory Pathologies Laboratory, School of Life Sciences, Central University of Gujarat, Sector -30, Gandhinagar, 382030, Gujarat, India. umeshyadav@cug.ac.in.
Central University of Gujarat · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acacetin, a bioflavanoid, contains anti-inflammatory and anti-cancer activities as shown in different experimental models. However, its anticancer potential and mechanism of action against colorectal cancer cells is largely unknown. Here, we have investigated the efficacy of acacetin using two colorectal adenocarcinoma SW480 and HCT-116 cell lines. Cell survival was examined by Trypan-blue exclusion and MTT assays, cell cycle analysis by FACS, apoptosis was assessed using Annexin V FITC assay and nuclear condensation by Hoechst staining, ROS level by DCFDA and Mitosox, and protein expression level by Western blotting. Acacetin reduced the cell survival and proliferation of both types of cells, and induced S- and G2-M phase arrest and also reduced the levels of β-catenin and its downstream target c-myc. Further, acacetin induced apoptosis as examined by Annexin-V FITC and nuclear condensation. It increased intracellular ROS production, especially mitochondrial ROS. Acacetin increased mitochondrial membrane potential depolarization and Bax:Bcl-2 ratio. Although significant changes in caspases -8 and -9 and PARP level was not observed, acacetin could induce the truncation and subsequent translocation of activated AIF from mitochondria to cytosol, which could further induce chromosomal breakage leading to apoptosis. In conclusion, Acacetin induces mitochondrial ROS-mediated cell death in a caspase-independent manner in SW480 and HCT-116 colon carcinoma cells by inducing apoptosis inducing factor (AIF), which may potentiate its anticancer and chemotherapeutic prospects against colorectal carcinoma.

Indexed as

Apoptosisbcl-2-Associated X Proteinbeta CateninCaspase 3Caspase 8CaspasesCell CycleCell Cycle CheckpointsCell Line, TumorCell ProliferationCell SurvivalColorectal NeoplasmsFlavonesHCT116 CellsHumansMitochondriaacacetinbcl-2-Associated X Proteinbeta CateninCaspase 3Caspase 8CaspasesFlavonesReactive Oxygen SpeciesAcacetinApoptosis inducing factorCaspase-independent apoptosisCell cycle arrestColon cancerOxidative stress

Identifiers

PMID31734898
OpenAlexW2986262397

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.