Evidence map›Paper›PMID 32979141›Full record

ArticleBiochemical genetics2021

Naringin Combined with NF-κB Inhibition and Endoplasmic Reticulum Stress Induces Apoptotic Cell Death via Oxidative Stress and the PERK/eIF2α/ATF4/CHOP Axis in HT29 Colon Cancer Cells.

Doğan Albayrak, Oğuzhan Doğanlar, Suat Erdoğan, Meryem Meraklı, Ayten Doğan, Pelin Turker, Ayten Bostancı, Zeynep Banu Doğanlar

Abstract read
PubMed Publisher
In one paragraph

Article in Biochemical genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

16 citing papers in PubMed, 44 citations in OpenAlex.

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  11. Review
  12. Naringin Prevents Cognitive Dysfunction in Aging Rats by Inhibiting Toll-Like Receptor 4 (TLR4)/NF-Evidence-based complementary and alternative medicine : eCAM · 2023
    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

8 authors at 1 institution in 1 country.

Doğan AlbayrakDepartment of Surgery, Faculty of Medicine, Trakya University, 22030, Edirne, Turkey.ORCID http://orcid.org/0000-0002-1950-2444
Oğuzhan DoğanlarDepartment of Medical Biology, Faculty of Medicine, Trakya University, 22030, Edirne, Turkey.ORCID http://orcid.org/0000-0003-2654-7269
Suat ErdoğanDepartment of Medical Biology, Faculty of Medicine, Trakya University, 22030, Edirne, Turkey.
Meryem MeraklıDepartment of Medical Biology, Faculty of Medicine, Trakya University, 22030, Edirne, Turkey.
Ayten DoğanDepartment of Medical Biology, Faculty of Medicine, Trakya University, 22030, Edirne, Turkey.
Pelin TurkerDepartment of Molecular Genetic Lab, Technology Research and Application Center, Trakya University, 22030, Edirne, Turkey.
Ayten BostancıDepartment of Genetic and Bioengineering, Faculty of Engineering, Trakya University, 22030, Edirne, Turkey.
Zeynep Banu DoğanlarDepartment of Medical Biology, Faculty of Medicine, Trakya University, 22030, Edirne, Turkey. zdoganlar@trakya.edu.tr.ORCID http://orcid.org/0000-0002-1365-9897
Trakya University · TR

Funding

Trakya Üniversitesi (TUBAP 2016/42)
6 · The paper itself

Abstract

Currently, combination therapy is considered the most effective solution for a selective chemotherapeutic effect in the treatment of colon cancer. This study investigated the death of both colon cancer HT29 cells and healthy vascular smooth muscle TG-Ha-VSMC cells (VSMCs) induced by naringin combined with endoplasmic reticulum (ER) stress and NF-κB inhibition. Naringin combined with tunicamycin and BAY 11-7082 suppressed the proliferation of HT29 cells in a dose-dependent manner and induced particularly apoptotic death without significantly affecting healthy VSMCs according to Annexin V/PI staining and AO/EB staining analyses. Insufficient antioxidant defense and heat shock response as well as excessive ROS generation were observed in HT29 cells following combination therapy. Quantitative real-time PCR and western blot analysis demonstrated that drug combination-induced mitochondrial apoptosis was activated through the ROS-mediated PERK/eIF2α/ATF4/CHOP pathway. Additionally, naringin combination significantly reduced the sXBP expression induced by tunicamycin+BAY 11-7082 in a dose-dependent manner. In conclusion, this study found that naringin combined with tunicamycin+BAY 11-7082 efficiently induced apoptotic cell death in HT29 colon cancer cells via oxidative stress and the PERK/eIF2α/ATF4/CHOP pathway, suggesting that naringin combined with tunicamycin plus BAY 11-7082 could be a new combination therapy strategy for effective colon cancer treatment with minimal side effects on healthy cells.

Indexed as

ApoptosisEndoplasmic Reticulum StressOxidative StressSignal TransductionActivating Transcription Factor 4AntioxidantsCaspasesCell Line, TumorCell SurvivalColonic NeoplasmseIF-2 KinaseEndoplasmic ReticulumEukaryotic Initiation Factor-2FlavanonesHT29 CellsHumans3-(4-methylphenylsulfonyl)-2-propenenitrileActivating Transcription Factor 4AntioxidantsATF4 protein, humanCaspasesDDIT3 protein, humanEIF2AK3 protein, humaneIF-2 KinaseEukaryotic Initiation Factor-2FlavanonesnaringinNF-kappa B p50 SubunitNFKB1 protein, humanNitrilesReactive Oxygen SpeciesSulfonesTranscription Factor CHOPTunicamycinApoptosisBAY 11-7082Colon cancerER stressNaringinTunicamycin

Identifiers

PMID32979141
OpenAlexW3088380631

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.