Evidence map›Paper›PMID 31611630›Full record

ArticleScientific reports2019

Silencing of Glutathione S-Transferase Pi Inhibits Cancer Cell Growth via Oxidative Stress Induced by Mitochondria Dysfunction.

Naoki Fujitani, Akihiro Yoneda, Motoko Takahashi, Akira Takasawa, Tomoyuki Aoyama, Tadaaki Miyazaki

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

9 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Review
  3. High-Dose Vitamin C for Cancer Therapy.Pharmaceuticals (Basel, Switzerland) · 2022
    Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. E2F1 sumoylation as a protective cellular mechanism in oxidative stress response.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  9. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Naoki FujitaniDepartment of Biochemistry, Sapporo Medical University School of Medicine, S1W17, Sapporo, 060-8556, Japan.
Akihiro YonedaDepartment of Molecular Therapeutics, Center for Food and Medical Innovation, Institute for the Promotion of Business-Regional Collaboration, Hokkaido University, N21W11, Sapporo, 001-0021, Japan. ayoneda@fmi.hokudai.ac.jp.
Motoko TakahashiDepartment of Biochemistry, Sapporo Medical University School of Medicine, S1W17, Sapporo, 060-8556, Japan.
Akira TakasawaDepartment of Pathology, Sapporo Medical University School of Medicine, S1W17, Sapporo, 060-8556, Japan.
Tomoyuki AoyamaDepartment of Pathology, Sapporo Medical University School of Medicine, S1W17, Sapporo, 060-8556, Japan.
Tadaaki MiyazakiDepartment of Probiotics Immunology, Institute for Genetic Medicine, Hokkaido University, N15W7, Sapporo, 001-0015, Japan.
Sapporo Medical University · JPHokkaido University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Antitumor drug development based on the concept of intervening in the antioxidant system of cancer cells has been gaining increased interest. In this study, we propose a promising strategy for cancer treatment using modulation of oxidative stress by suppression of glutathione S-transferases (GSTs), a typical antioxidant enzyme. siRNA which can be applied to the development of nucleic acid drugs, enabling them to eliminate unwanted side effects, increase specificity, and avoid the problem of drug resistance, was employed for GSTP-silencing at the transcriptional level. The silencing of the pi class of GST (GSTP) that displayed the most characteristic expression profile in 13 kinds of cancer cell lines has shown significant impairment in the growth of cancer cells due to oxidative stress caused by excess ROS accumulation. Comparative proteomics between normal cells and GSTP-silenced pancreatic cancer cell PANC-1 suggested that GSTP-silencing facilitated the mitochondrial dysfunction. These findings show promise for the development of strategies toward cancer therapy based on the mechanism that allows genetic silencing of GSTP to promote oxidative stress through mitochondria dysfunction.

Indexed as

Oxidative StressCell Line, TumorCell ProliferationGlutathione S-Transferase piHumansMitochondriaPancreatic NeoplasmsRNA InterferenceRNAi TherapeuticsRNA, Small InterferingGlutathione S-Transferase piGSTP1 protein, humanRNA, Small Interfering

Identifiers

PMID31611630
PMCPMC6791853
OpenAlexW2979538008

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.