Evidence map›Paper›PMID 30464531›Full record

ArticleOncoTargets and therapy2018

TRIM32 overexpression improves chemoresistance through regulation of mitochondrial function in non-small-cell lung cancers.

Yaming Du, Wei Zhang, Binghui Du, Sheng Zang, Xinpeng Wang, Xin Mao, Zhansheng Hu

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Cancer-Associated Dysregulation of Sumo Regulators: Proteases and Ligases.International journal of molecular sciences · 2022
    Review
  7. Article
  8. The Role of SUMO E3 Ligases in Signaling Pathway of Cancer Cells.International journal of molecular sciences · 2022
    Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Review
  15. Article
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

7 authors at 1 institution in 1 country.

Yaming DuDepartment of Vascular Surgery, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, Liaoning, China.
Wei ZhangDepartment of Vascular Surgery, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, Liaoning, China.
Binghui DuDepartment of Vascular Surgery, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, Liaoning, China.
Sheng ZangDepartment of Vascular Surgery, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, Liaoning, China.
Xinpeng WangDepartment of Vascular Surgery, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, Liaoning, China.
Xin MaoDepartment of Vascular Surgery, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, Liaoning, China.
Zhansheng HuDepartment of Intensive Care Unit, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, Liaoning, China, bubu3473354703@163.com.
Jinzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTRIM32 is overexpressed in several human cancers. However, its expression pattern, biological characteristics and mechanisms in human non-small cell lung cancer (NSCLC) have not been reported.

methodsWe examined TRIM32 protein in 115 cases of NSCLC specimens. TRIM32 plasmid transfection and siRNA knockdown was carried out in NSCLC cell lines. AnnexinV/PI and JC-1 staining were performed to examine the change of apoptosis and mitochondrial membrane potential. Western blot was used to detect change of downstream proteins.

resultsWe found that TRIM32 protein was upregulated in 69 cases and positively correlated with advanced TNM stage. TRIM32 overexpression also correlated with poor survival of NSCLC patients. Biological assays demonstrated that TRIM32 overexpression promoted while it depletion inhibited cell growth, colony formation and invasion. In addition, TRIM32 maintained NSCLC cell viability and reduced apoptosis when treated with cisplatin. JC-1 and CellRox staining demonstrated that TRIM32 could maintain mitochondrial membrane potential and reduce Reactive Oxygen Species (ROS) production after cisplatin treatment. Western blot analysis showed that TRIM32 overexpression downregulated caspase 3 cleavage and cytochrome c release. TRIM32 also positively regulated Bcl-2 protein expression and NF-κB signaling. Inhibition of NF-κB abolished the effects of TRIM32 on Bcl-2.

conclusionTaken together, our results indicated that TRIM32 is overexpressed in NSCLC and regulates cisplatin resistance, possibly through NF-κB and Bcl-2.

Indexed as

apoptosisNF-κBNSCLCTRIM32

Identifiers

PMID30464531
PMCPMC6225845
OpenAlexW2898890778

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.