Evidence map›Paper›PMID 31011292›Full record

ArticleCancer cell international2019

Emodin inhibits colon cancer by altering BCL-2 family proteins and cell survival pathways.

Ian T Saunders, Hina Mir, Neeraj Kapur, Shailesh Singh

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
11.0field-weighted citation impact, top 2% 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

31 citing papers in PubMed, 56 citations in OpenAlex.

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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

4 authors at 1 institution in 1 country.

Ian T Saunders1Department of Microbiology, Biochemistry and Immunology and Cancer Health Equity Institute, Morehouse School of Medicine, Atlanta, GA 30310 USA.
Hina Mir1Department of Microbiology, Biochemistry and Immunology and Cancer Health Equity Institute, Morehouse School of Medicine, Atlanta, GA 30310 USA.
Neeraj Kapur1Department of Microbiology, Biochemistry and Immunology and Cancer Health Equity Institute, Morehouse School of Medicine, Atlanta, GA 30310 USA.
Shailesh Singh1Department of Microbiology, Biochemistry and Immunology and Cancer Health Equity Institute, Morehouse School of Medicine, Atlanta, GA 30310 USA.
Morehouse School of Medicine · US

Funding

Training the Trainers: Building Institutional Data Science Capacity to Support Health Disparities ResearchU54MD007602 · NIMHD · MOREHOUSE SCHOOL OF MEDICINE · PI Kevin Sean Kimbro · 2018 to 2026
$47.6M
Research Training & Career Development ProgramU54CA118638 · NCI · MOREHOUSE SCHOOL OF MEDICINE · PI James W Lillard, Brian M. Rivers · 2005 to 2026
$22.7M
Role of CCL25-CCR9 in Prostate CancerSC1CA180212 · NCI · MOREHOUSE SCHOOL OF MEDICINE · PI SINGH, SHAILESH · 2013 to 2017
$1.8M
Role of chemokine receptor in disparities associated with prostate cancer progresU01CA179701 · NCI · MOREHOUSE SCHOOL OF MEDICINE · PI SINGH, SHAILESH · 2013 to 2017
$822k
Prostate Cancer Chemoprevention using a Natural AgentR21CA169716 · NCI · MOREHOUSE SCHOOL OF MEDICINE · PI SINGH, SHAILESH · 2013 to 2014
$334k
NCI NIH HHS R21 CA169716NCI NIH HHS SC1 CA180212NCI NIH HHS U01 CA179701NCI NIH HHS U54 CA118638NIMHD NIH HHS U54 MD007602
6 · The paper itself

Abstract

backgroundCurrently offered therapeutics to treat colon cancer (CoCa) are toxic when given at maximum tolerated dose to achieve optimal clinical response. Hence, less toxic therapeutic intervention is needed to treat CoCa. In this study, we investigated the effect of a natural agent, Emodin, on CoCa.

methodsCell viability (MTT) assay was used to determine the effect of Emodin on human CoCa and colon epithelial cells. Flow cytometric analysis was used to determine Emodin induced cell death. Antibody microarray and western blot analyses were used to determine Emodin induced molecular changes involved in cell death. Change in mitochondrial membrane potential in response to Emodin was determined by flow cytometric analysis. Expression and localization of Bcl-2 family proteins were assessed by western blot analysis.

resultsEmodin decreased viability of CoCa cells and induced apoptosis in a time and dose-dependent manner compared to vehicle-treated control without significantly impacting normal colon epithelial cells. Emodin activated caspases, modulated Bcl-2 family of proteins and reduced mitochondrial membrane potential to induce CoCa cell death. Further, changes in Bcl-2 family protein expression and localization correlated with loss in mitochondrial membrane potential. Signaling (MAPK/JNK, PI3K/AKT, NF-κβ and STAT) pathways associated with cell growth, differentiation, and Bcl-2 family expression or function were negatively regulated by Emodin.

conclusionsAbility of Emodin to impact molecular pathways involved in cell survival and apoptosis highlight the potential of this agent as a new and less toxic alternative for CoCa treatment.

Indexed as

AnthraquinoneApoptosisBcl-2Colon cancerEmodinMitochondria

Identifiers

PMID31011292
PMCPMC6466701
OpenAlexW2945513881

What Socratic 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 Socratic graph.