Evidence map›Paper›PMID 33786632›Full record

ArticleMolecular medicine reports2021

ABT‑737, a Bcl‑2 family inhibitor, has a synergistic effect with apoptosis by inducing urothelial carcinoma cell necroptosis.

Rui Cheng, Xiaolong Liu, Zheng Wang, Kunlong Tang

RetractedOpen access · hybridAbstract readRetracted Publication
In one paragraph

Article in Molecular medicine reports, 2021. 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 It has been retracted, and should not be counted.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 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

13 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. ZBP1 and heatstroke.Frontiers in immunology · 2023
    Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Regulated Cell Death in Urinary Malignancies.Frontiers in cell and developmental biology · 2021
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Rui ChengDepartment of Urology, Tianjin Medical University General Hospital, Tianjin 300052, P.R. China.
Xiaolong LiuDepartment of Urology, Tianjin Medical University General Hospital, Tianjin 300052, P.R. China.
Zheng WangDepartment of Surgery, Tianjin Medical University General Hospital, Tianjin 300052, P.R. China.
Kunlong TangDepartment of Urology, Tianjin Medical University General Hospital, Tianjin 300052, P.R. China.
Tianjin Medical University General Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

ABT‑737 is a recently reported inhibitor of members of the Bcl‑2 family of apoptosis regulators. However, to the best of our knowledge, its necroptosis‑inducing function in bladder cancer has not yet been researched. Thus, the present study aimed to investigate whether this Bcl‑2 family inhibitor can induce both apoptosis and necroptosis of urothelial carcinoma cells. The proliferation and survival of urothelial carcinoma cell lines treated with a combination of both Z‑VAD‑FMK as a pan‑caspase inhibitor and ABT‑737 were assessed in vitro. Z‑DNA binding protein 1 (ZBP1), receptor‑interacting protein (RIP)1 and RIP3 were knocked down using small interfering RNA in urothelial carcinoma cell lines. The protein expression levels of ZBP1, RIP1 and RIP3 following cell transfection were measured via western blot analysis. Cell viability was determined using an MTT assay. Cell invasion was examined using cell invasion assays. The expression levels of necroptosis‑related proteins, high mobility group box 1, ZBP1, mixed‑lineage kinase domain‑like protein (MLKL) and RIP3, were measured via western blotting. It was found that ABT‑737 inhibited the proliferation and invasion of bladder cancer cells by inducing cell necrosis. The data demonstrated that ZBP1 and RIP3 have main roles in the cell necrosis induced by ABT‑737. In addition, RIP3 and ZBP1, without interacting with RIP1, directly induced MLKL‑mediated programmed cell necrosis. Thus, understanding how urothelial carcinoma cells react to Bcl‑2 family inhibitors may accelerate the discovery of drugs to treat bladder cancer.

Indexed as

ApoptosisAntineoplastic AgentsBiphenyl CompoundsCarcinomaCell Line, TumorHumansNecroptosisNitrophenolsNuclear Pore Complex ProteinsPiperazinesProtein KinasesProto-Oncogene Proteins c-bcl-2Receptor-Interacting Protein Serine-Threonine KinasesRNA-Binding ProteinsSulfonamidesUrinary Bladder NeoplasmsABT-737AGFG1 protein, humanAntineoplastic AgentsBiphenyl CompoundsMLKL protein, humanNitrophenolsNuclear Pore Complex ProteinsPiperazinesProtein KinasesProto-Oncogene Proteins c-bcl-2Receptor-Interacting Protein Serine-Threonine KinasesRIPK3 protein, humanRNA-Binding ProteinsSulfonamidesZBP1 protein, humanapoptosisnecroptosisurothelial carcinoma cells

Identifiers

PMID33786632
PMCPMC8025475
OpenAlexW3147046801

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.