Evidence map›Paper›PMID 37219768›Full record

ArticleCellular oncology (Dordrecht, Netherlands)2023

TRIM17-mediated ubiquitination and degradation of RBM38 promotes cisplatin resistance in non-small cell lung cancer.

Tian Zhong, Jing Zhang, Xingren Liu, Hongmin Li

Abstract read
In one paragraph

Article in Cellular oncology (Dordrecht, Netherlands), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
3.5field-weighted citation impact, top 7% 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, 15 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. The cross talk of ubiquitination and chemotherapy tolerance in colorectal cancer.Journal of cancer research and clinical oncology · 2024
    Review
  11. Article
  12. Is MG53 a potential therapeutic target for cancer?Frontiers in endocrinology · 2023
    Review
  13. Review
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

4 authors at 2 institutions in 1 country.

Tian ZhongDepartment of Pulmonary and Critical Care Medicine, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, China.
Jing ZhangDepartment of Pulmonary and Critical Care Medicine, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, China.
Xingren LiuDepartment of Pulmonary and Critical Care Medicine, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, China. tomsan2022@126.com.
Hongmin LiChinese Academy of Sciences Sichuan Translational Medicine Research Hospital, Chengdu, China. lihongmin@med.uestc.edu.cn.
University of Electronic Science and Technology of China · CNSichuan Academy of Traditional Chinese Medicine · CN

Funding

Research Foundation from Sichuan Provincial Health and Family Planning Commission of China 17PJ039
6 · The paper itself

Abstract

Cisplatin (CDDP)-based chemotherapy is commonly used to treat advanced non-small cell lung cancer (NSCLC). However, the efficacy is limited by the development of drug resistance. Tripartite motif (TRIM) proteins typically have E3 ubiquitin ligase activities and modulate protein stability. In the present study, we screened for chemosensitivity-regulating TRIM proteins using CDDP-resistant NSCLC cell lines. We show that TRIM17 is upregulated in CDDP-resistant NSCLC cells and tumors compared to CDDP-sensitive counterparts. NSCLC patients with high TRIM17 expression in tumors have shorter progression-free survival than those with low TRIM17 expression after CDDP chemotherapy. Knockdown of TRIM17 increases the sensitivity of NSCLC cells to CDDP both in vitro and in vivo. In contrast, overexpression of TRIM17 promotes CDDP resistance in NSCLC cells. TRIM17-mediated CDDP resistance is associated with attenuation of reactive oxygen species (ROS) production and DNA damage. Mechanistically, TRIM17 interacts with RBM38 and promotes K48-linked ubiquitination and degradation of RBM38. TRIM17-induced CDDP resistance is remarkably reversed by RBM38. Additionally, RBM38 enhances CDDP-induced production of ROS. In conclusion, TRIM17 upregulation drives CDDP resistance in NSCLC largely by promoting RBM38 ubiquitination and degradation. Targeting TRIM17 may represent a promising strategy for improving CDDP-based chemotherapy in NSCLC.

Indexed as

Antineoplastic AgentsCarcinoma, Non-Small-Cell LungLung NeoplasmsCell Line, TumorCisplatinDrug Resistance, NeoplasmHumansReactive Oxygen SpeciesRNA-Binding ProteinsTripartite Motif ProteinsUbiquitinationUbiquitin-Protein LigasesAntineoplastic AgentsCisplatinRBM38 protein, humanReactive Oxygen SpeciesRNA-Binding ProteinsTRIM17 protein, humanTripartite Motif ProteinsUbiquitin-Protein LigasesDrug resistanceLung cancerOxidative stressRBM38TRIM17

Identifiers

PMID37219768
PMCPMC12974751
OpenAlexW4377565489

What OpenQuestion holds

Textmetadata
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.