Evidence map›Paper›PMID 28412728›Full record

ArticleOncotarget2017

Increased reactive oxygen species levels cause ER stress and cytotoxicity in andrographolide treated colon cancer cells.

Aditi Banerjee, Vivekjyoti Banerjee, Steven Czinn, Thomas Blanchard

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
20.4field-weighted citation impact, top 1% 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

59 citing papers in PubMed, 98 citations in OpenAlex.

  1. Article
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  11. Cytotoxic Effect ofCurrent issues in molecular biology · 2024
    Article
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  15. Review
  16. Phytochemical Analysis and Anticancer Properties ofMolecules (Basel, Switzerland) · 2023
    Article
  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

4 authors at 1 institution in 1 country.

Aditi BanerjeeDepartment of Pediatrics, University of Maryland School of Medicine, Baltimore, Maryland, U.S.A.
Vivekjyoti BanerjeeDepartment of Pediatrics, University of Maryland School of Medicine, Baltimore, Maryland, U.S.A.
Steven CzinnDepartment of Pediatrics, University of Maryland School of Medicine, Baltimore, Maryland, U.S.A.
Thomas BlanchardDepartment of Pediatrics, University of Maryland School of Medicine, Baltimore, Maryland, U.S.A.
University of Maryland, Baltimore · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chemotherapy continues to play an essential role in the management of many cancers including colon cancer, the third leading cause of death due to cancer in the United States. Many naturally occurring plant compounds have been demonstrated to possess anti-cancer cell activity and have the potential to supplement existing chemotherapy strategies. The plant metabolite andrographolide induces cell death in cancer cells and apoptosis is dependent upon the induction of endoplasmic reticulum stress (ER stress) leading to the unfolded protein response (UPR). The goal of the present study was to determine the mechanism by which andrographolide induces ER stress and to further evaluate its role in promoting cell death pathways. The T84 and COLO 205 cancer cell lines were used to demonstrate that andrographolide induces increased ROS levels, corresponding anti-oxidant response molecules, and reduced mitochondrial membrane potential. No increases in ROS levels were detected in control colon fibroblast cells. Andrographolide-induced cell death, UPR signaling, and CHOP, Bax, and caspase 3 apoptosis elements were all inhibited in the presence of the ROS scavenger NAC. Additionally, andrographolide-induced suppression of cyclins B1 and D1 were also reversed in the presence of NAC. Finally, Akt phosphorylation and phospho-mTOR levels that are normally suppressed by andrographolide were also expressed at normal levels in the absence of ROS. These data demonstrate that andrographolide induces ER stress leading to apoptosis through the induction of ROS and that elevated ROS also play an important role in down-regulating cell cycle progression and cell survival pathways as well.

Indexed as

Antineoplastic AgentsAntioxidantsApoptosisCell Cycle CheckpointsCell Line, TumorCell ProliferationCell SurvivalColonic NeoplasmsDiterpenesEndoplasmic Reticulum StressGene Expression Regulation, NeoplasticHumansMembrane Potential, MitochondrialOxidation-ReductionOxidative StressReactive Oxygen SpeciesandrographolideAntineoplastic AgentsAntioxidantsDiterpenesReactive Oxygen Speciesandrographolidechemotherapyendoplasmic reticulum stressreactive oxygen speciesunfolded protein response

Identifiers

PMID28412728
PMCPMC5432246
OpenAlexW2588583241

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.