Evidence map›Paper›PMID 31482012›Full record

ArticleCell death discovery2019

Transcription-independent and -dependent p53-mediated apoptosis in response to genotoxic and non-genotoxic stress.

Cheng-Jung Ho, Ru-Wei Lin, Wei-Hua Zhu, Tsung-Kai Wen, Chieh-Ju Hu, Yi-Lin Lee, Ta-I Hung, Chihuei Wang

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.1field-weighted citation impact, top 11% 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

22 citing papers in PubMed, 37 citations in OpenAlex.

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  19. Toxicity and Anti-Proliferative Properties ofLife (Basel, Switzerland) · 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

8 authors at 4 institutions in 1 country.

Cheng-Jung Ho *1Department of Orthopedics, Kaohsiung Medical University Hospital, 80708 Kaohsiung, Taiwan.
Ru-Wei Lin *2Graduate Institute of Food Safety Management, National Pingtung University of Science and Technology, 91201 Pingtung, Taiwan.
Wei-Hua Zhu *3Department of Biotechnology, Kaohsiung Medical University, 80708 Kaohsiung, Taiwan.
Tsung-Kai Wen4School of Post-Baccalaureate Chinese Medicine, Tzu Chi University, 97004 Hualien, Taiwan.
Chieh-Ju Hu3Department of Biotechnology, Kaohsiung Medical University, 80708 Kaohsiung, Taiwan.
Yi-Lin Lee3Department of Biotechnology, Kaohsiung Medical University, 80708 Kaohsiung, Taiwan.
Ta-I Hung3Department of Biotechnology, Kaohsiung Medical University, 80708 Kaohsiung, Taiwan.
Chihuei Wang3Department of Biotechnology, Kaohsiung Medical University, 80708 Kaohsiung, Taiwan.
Kaohsiung Medical University · TWKaohsiung Medical University Chung-Ho Memorial Hospital · TWNational Pingtung University of Science and Technology · TWTzu Chi University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We previously reported that p53-mediated apoptosis is determined by severity of DNA damage, not by the level of p53, in doxorubicin-treated prostate cancer cells. In addition to doxorubicin, our results here indicated that camptothecin and bortezomib, which are a topoisomerase 1 poison and a 26 S proteasome inhibitor, respectively, could also induce apoptosis in a p53-dependent manner in prostate cancer. Then, we examined whether p53-mediated apoptosis induced by genotoxic and non-genotoxic stress occur in the same or a different way. By using dominant negative p53 to compete with wild-type p53 in transcription activity, we demonstrated that p53-mediated apoptosis in response to doxorubicin- or camptothecin-induced genotoxic stress is transcription-independent. In contrast, p53-mediated apoptosis from bortezomib-induced stress is transcription-dependent. Interestingly, we also found that doxorubicin-induced p21 expression is activated by p53 in transcription-dependent manner, while camptothecin-induced p21 expression is p53-independent. We then investigated the p53 ratio of nucleus to cytosol corresponding to low and high dose doxorubicin, camptothecin, or bortezomib treatment. The results suggested that p53 translocation from cytoplasm to nucleus actively drives cells toward apoptosis in either transcription-dependent or -independent manner for responding to non-genotoxic or genotoxic stress, respectively.

Indexed as

ApoptosisStress signalling

Identifiers

PMID31482012
PMCPMC6711993
OpenAlexW2971235293

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.