Evidence map›Paper›PMID 28796811›Full record

ArticlePloS one2017

Biphasic ROS production, p53 and BIK dictate the mode of cell death in response to DNA damage in colon cancer cells.

Ozgur Kutuk, Nurgul Aytan, Bahriye Karakas, Asli Giray Kurt, Ufuk Acikbas, Sehime Gulsun Temel, Huveyda Basaga

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

13 citing papers in PubMed, 40 citations in OpenAlex.

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  9. Chiauranib selectively inhibits colorectal cancer withAmerican journal of cancer research · 2020
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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

7 authors at 4 institutions in 3 countries.

Ozgur KutukDepartment of Medical Genetics, Baskent University School of Medicine, Adana Dr. Turgut Noyan Medical and Research Center, Adana, Turkey.ORCID http://orcid.org/0000-0001-9854-7220
Nurgul AytanDepartment of Neurology, Boston University School of Medicine, Boston, United States of America.
Bahriye KarakasMolecular Biology, Genetics and Bioengineering Program, Sabanci University, Istanbul, Turkey.
Asli Giray KurtDepartment of Medical Genetics, Baskent University School of Medicine, Adana Dr. Turgut Noyan Medical and Research Center, Adana, Turkey.
Ufuk AcikbasDepartment of Medical Genetics, Baskent University School of Medicine, Adana Dr. Turgut Noyan Medical and Research Center, Adana, Turkey.
Sehime Gulsun TemelDepartment of Histology and Embryology, Uludag University School of Medicine, Bursa, Turkey.
Huveyda BasagaMolecular Biology, Genetics and Bioengineering Program, Sabanci University, Istanbul, Turkey.
Başkent University · TRSabancı Üniversitesi · TRBoston University · USBursa Uludağ Üni̇versi̇tesi̇ · TR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Necrosis, apoptosis and autophagic cell death are the main cell death pathways in multicellular organisms, all with distinct and overlapping cellular and biochemical features. DNA damage may trigger different types of cell death in cancer cells but the molecular events governing the mode of cell death remain elusive. Here we showed that increased BH3-only protein BIK levels promoted cisplatin- and UV-induced mitochondrial apoptosis and biphasic ROS production in HCT-116 wild-type cells. Nonetheless, early single peak of ROS formation along with lysosomal membrane permeabilization and cathepsin activation regulated cisplatin- and UV-induced necrosis in p53-null HCT-116 cells. Of note, necrotic cell death in p53-null HCT-116 cells did not depend on BIK, mitochondrial outer membrane permeabilization or caspase activation. These data demonstrate how cancer cells with different p53 background respond to DNA-damaging agents by integrating distinct cell signaling pathways dictating the mode of cell death.

Indexed as

ApoptosisDNA DamageAntineoplastic AgentsApoptosis Regulatory ProteinsCisplatinColonic NeoplasmsHCT116 CellsHumansLysosomesMembrane PotentialsMembrane ProteinsMitochondrial ProteinsReactive Oxygen SpeciesTumor Suppressor Protein p53Antineoplastic AgentsApoptosis Regulatory ProteinsBIK protein, humanCisplatinMembrane ProteinsMitochondrial ProteinsReactive Oxygen SpeciesTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID28796811
PMCPMC5552129
OpenAlexW2742384749

What OpenQuestion holds

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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.