Evidence map›Paper›PMID 31347653›Full record

ArticleJournal of radiation research2019

WEE1 inhibition enhances sensitivity to hypoxia/reoxygenation in HeLa cells.

Tatsuaki Goto, Hisao Homma, Atsushi Kaida, Masahiko Miura

Erratum issuedOpen access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of radiation research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.1field-weighted citation impact, top 52% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Tatsuaki GotoDepartment of Oral Radiation Oncology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo, Japan.
Hisao HommaDepartment of Oral Radiation Oncology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo, Japan.
Atsushi KaidaDepartment of Oral Radiation Oncology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo, Japan.
Masahiko MiuraDepartment of Oral Radiation Oncology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo, Japan.
Tokyo Medical and Dental University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypoxia/reoxygenation (H/R) treatment reportedly induces DNA damage response (DDR), including DNA double-strand break (DSB) repair and G2 arrest, resulting in reduction of clonogenic survival. Because WEE1 plays a key role in the G2/M checkpoint along with CHK1/2, we investigated the effect of WEE1 inhibition on H/R-induced DDR using HeLa cells. The H/R treatment combined with WEE1 inhibitor abrogated G2 arrest, subsequently leading to the cells entering the M phase, and finally resulting in mitotic catastrophe after prolonged mitosis. Colony-forming assay showed an enhanced decrease in the surviving fraction and the focus formation of BRCA1 was significantly reduced. We demonstrate for the first time that WEE1 inhibition enhances H/R-induced cell death accompanied by mitotic catastrophe and that the process may be mediated by homologous recombination.

Indexed as

BRCA1 ProteinCell Cycle ProteinsCell HypoxiaCell SurvivalClone CellsG2 Phase Cell Cycle CheckpointsHeLa CellsHumansKineticsMitosisOxygenProtein-Tyrosine KinasesPyrazolesPyrimidinonesadavosertibBRCA1 ProteinBRCA1 protein, humanCell Cycle ProteinsOxygenProtein-Tyrosine KinasesPyrazolesPyrimidinonesWEE1 protein, humanDNA double-strand breakshomologous recombinationhypoxiareoxygenationWEE1

Identifiers

PMID31347653
PMCPMC6805980
OpenAlexW2981600657

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.