Evidence map›Paper›PMID 32377739›Full record

ArticleMolecular medicine reports2020

p53/PGC‑1α‑mediated mitochondrial dysfunction promotes PC3 prostate cancer cell apoptosis.

Jiuling Li, Yany Li, Lanlan Chen, Bingbing Yu, Yanan Xue, Rui Guo, Jing Su, Yanan Liu, Liankun Sun

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

21 citing papers in PubMed, 27 citations in OpenAlex.

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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

9 authors at 1 institution in 1 country.

Jiuling LiDepartment of Pathophysiology, Prostate Diseases Prevention and Treatment Research Center, College of Basic Medical Sciences, Jilin University, Changchun, Jilin 130021, P.R. China.
Yany LiDepartment of Pathophysiology, Prostate Diseases Prevention and Treatment Research Center, College of Basic Medical Sciences, Jilin University, Changchun, Jilin 130021, P.R. China.
Lanlan ChenSchool of Clinical Medicine, Jilin University, Changchun, Jilin 130021, P.R. China.
Bingbing YuDepartment of Pathophysiology, Prostate Diseases Prevention and Treatment Research Center, College of Basic Medical Sciences, Jilin University, Changchun, Jilin 130021, P.R. China.
Yanan XueDepartment of Pathophysiology, Prostate Diseases Prevention and Treatment Research Center, College of Basic Medical Sciences, Jilin University, Changchun, Jilin 130021, P.R. China.
Rui GuoDepartment of Pathophysiology, Prostate Diseases Prevention and Treatment Research Center, College of Basic Medical Sciences, Jilin University, Changchun, Jilin 130021, P.R. China.
Jing SuDepartment of Pathophysiology, Prostate Diseases Prevention and Treatment Research Center, College of Basic Medical Sciences, Jilin University, Changchun, Jilin 130021, P.R. China.
Yanan LiuDepartment of Pathophysiology, Prostate Diseases Prevention and Treatment Research Center, College of Basic Medical Sciences, Jilin University, Changchun, Jilin 130021, P.R. China.
Liankun SunDepartment of Pathophysiology, Prostate Diseases Prevention and Treatment Research Center, College of Basic Medical Sciences, Jilin University, Changchun, Jilin 130021, P.R. China.
Jilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Data for p53 mutation in prostate cancer in The Cancer Genome Atlas database revealed that >85% of p53 mutations occurred in the p53 DNA binding domain. These mutations not only severely damage the function of the p53 protein, but also reduce the disease‑free survival of patients. Peroxisome proliferator‑activated receptor γ coactivator‑1α (PGC‑1α) is involved in the regulation of mitochondrial function and is highly expressed in prostate cancer PC3 and DU145 cells with p53 deletion or mutation. However, whether p53 negatively regulates PGC‑1α in prostate cancer cells remains to be elucidated. In the present study, p53 overexpression was induced in prostate cancer PC3 cells. Subsequently, the expression levels of PGC‑1α and alterations to mitochondrial function were assessed. Moreover, PGC‑1α was activated in prostate cancer PC3 cells using ZLN005 to investigate alterations to mitochondrial function and cell apoptosis. The present study revealed that p53 decreased the expression and nuclear localization of the PGC‑1α protein and induced mitochondrial dysfunction. Activation of PGC‑1α partially reversed p53‑mediated mitochondrial dysfunction. Inhibition of the p53/PGC‑1α pathway on mitochondrial biogenesis and fission‑/fusion‑associated gene and protein expression were associated with mitochondrial dysfunction. p53/PGC‑1α‑mediated mitochondrial dysfunction promoted apoptosis of PC3 prostate cancer cells. The results indicated that PGC‑1α is an essential target of p53‑induced apoptosis in prostate cancer cells and indicated that targeting PGC‑1α may provide a new therapeutic strategy for prostate cancer.

Indexed as

ApoptosisHumansMaleMitochondriaPC-3 CellsPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaProstatic NeoplasmsTumor Suppressor Protein p53Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPPARGC1A protein, humanTP53 protein, humanTumor Suppressor Protein p53apoptosismitochondriap53peroxisome proliferator-activated receptor γ coactivator-1αprostate cancerZln005

Identifiers

PMID32377739
PMCPMC7248533
OpenAlexW3023541224

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.