Evidence map›Paper›PMID 27666201›Full record

ArticleInternational journal of oncology2016

Mitomycin C and decarbamoyl mitomycin C induce p53-independent p21WAF1/CIP1 activation.

Shu-Yuan Cheng, Jiwon Seo, Bik Tzu Huang, Tanya Napolitano, Elise Champeil

Open access · hybridAbstract read
In one paragraph

Article in International journal of oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.3field-weighted citation impact, top 18% 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

19 citing papers in PubMed, 30 citations in OpenAlex.

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  10. Synthesis of Oligonucleotides Containing Trans Mitomycin C DNA Adducts at NChemistry (Weinheim an der Bergstrasse, Germany) · 2021
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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

5 authors at 2 institutions in 1 country.

Shu-Yuan ChengDepartment of Sciences, John Jay College of Criminal Justice, City University of New York, NY 10019, USA.
Jiwon SeoDepartment of Sciences, John Jay College of Criminal Justice, City University of New York, NY 10019, USA.
Bik Tzu HuangDepartment of Sciences, John Jay College of Criminal Justice, City University of New York, NY 10019, USA.
Tanya NapolitanoDepartment of Sciences, John Jay College of Criminal Justice, City University of New York, NY 10019, USA.
Elise ChampeilDepartment of Sciences, John Jay College of Criminal Justice, City University of New York, NY 10019, USA.
City University of New York · USJohn Jay College of Criminal Justice · US

Funding

Role of p21 signaling pathway in response to MC & DMC DNA Interstrand CrosslinksSC3GM105460 · NIGMS · JOHN JAY COLLEGE OF CRIMINAL JUSTICE · PI CHAMPEIL, ELISE · 2014 to 2022
$1.2M
NIGMS NIH HHS SC3 GM105460
6 · The paper itself

Abstract

Mitomycin C (MC), a commonly used anticancer drug, induces DNA damage via DNA alkylation. Decarbamoyl mitomycin C (DMC), another mitomycin lacking the carbamate at C10, generates similar lesions as MC. Interstrand cross-links (ICLs) are believed to be the lesions primarily responsible for the cytotoxicity of MC and DMC. The major ICL generated by MC (α-ICL) has a trans stereochemistry at the guanine-drug linkage whereas the major ICL from DMC (β-ICL) has the opposite, cis, stereochemistry. In addition, DMC can provoke strong p53-independent cell death. Our hypothesis is that the stereochemistry of the major unique β-ICL generated by DMC is responsible for this p53-independent cell death signaling. p53 gene is inactively mutated in more than half of human cancers. p21WAF1/CIP1 known as a major effector of p53 is involved in p53-dependent and -independent control of cell proliferation and death. This study revealed the role of p21WAF1/CIP1 on MC and DMC triggered cell damage. MCF-7 (p53-proficient) and K562 (p53-deficient) cells were used. Cell cycle distributions were shifted to the G1/S phase in MCF-7 treated with MC and DMC, but were shifted to the S phase in K562. p21WAF1/CIP1 activation was observed in both cells treated with MC and DMC, and DMC triggered more significant activation. Knocking down p53 in MCF-7 did not attenuate MC and DMC induced p21WAF1/CIP1 activation. The α-ICL itself was enough to cause p21WAF1/CIP1 activation.

Indexed as

Antibiotics, AntineoplasticApoptosisBlotting, WesternCell CycleCell ProliferationCyclin-Dependent Kinase Inhibitor p21Gene Expression Regulation, NeoplasticHumansK562 CellsMCF-7 CellsMitomycinTumor Suppressor Protein p53Antibiotics, AntineoplasticCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21MitomycinTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID27666201
PMCPMC5063421
OpenAlexW2522588995

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.