Evidence map›Paper›PMID 23358872›Full record

ArticleNeoplasia (New York, N.Y.)2013

The HECTD3 E3 ubiquitin ligase suppresses cisplatin-induced apoptosis via stabilizing MALT1.

Yi Li, Xi Chen, Zehua Wang, Dong Zhao, Hui Chen, Wenlin Chen, Zhongmei Zhou, Junran Zhang, Jing Zhang, Hongmin Li and 1 more

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

24 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Targeting HECTD3-IKKα axis inhibits inflammation-related metastasis.Signal transduction and targeted therapy · 2022
    Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. The role of E3 ubiquitin ligase HECTD3 in cancer and beyond.Cellular and molecular life sciences : CMLS · 2020
    Review
  18. Article
  19. Article
  20. 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

11 authors at 8 institutions in 2 countries.

Yi LiKey Laboratory of Animal Models and Human Disease Mechanisms of Chinese Academy of Sciences & Yunnan Province, Kunming Institute of Zoology, Kunming, Yunnan, China.
Xi Chen
Zehua Wang
Dong Zhao
Hui Chen
Wenlin Chen
Zhongmei Zhou
Junran Zhang
Jing Zhang
Hongmin Li
Ceshi Chen
Chinese Academy of Sciences · CNKunming Institute of Zoology · CNWadsworth Center · USAlbany Medical Center Hospital · USAlbany State University · USCase Western Reserve University · USChinese Academy of Medical Sciences & Peking Union Medical College · CNKunming Medical University · CN

Funding

THE ROLE OF NEDD4-1 IN IGF-1R SIGNALINGR01CA154625 · NCI · WASHINGTON UNIVERSITY · PI ZHANG, JUNRAN · 2011 to 2016
$1.6M
NCI NIH HHS R01 CA154625NCI NIH HHS R01CA154625
6 · The paper itself

Abstract

Homologous to the E6-associated protein carboxyl terminus domain containing 3 (HECTD3) is an E3 ubiquitin ligase with unknown functions. Here, we show that HECTD3 confers cancer cell resistance to cisplatin. To understand the molecular mechanisms, we performed a yeast two-hybrid analysis and identified mucosa-associated lymphoid tissue 1 (MALT1) as an HECTD3-interacting protein. HECTD3 promotes MALT1 ubiquitination with nondegradative polyubiquitin chains by direct interacting with the MALT1 through its N-terminal destruction of cyclin domain. HECTD3 does not target MALT1 for degradation but stabilize it. HECTD3 depletion dramatically decreases the levels of MALT1 in MCF7 and HeLa cells treated with cisplatin, which is correlated to an increase in apoptosis. Knockdown of MALT1 likewise increases cisplatin-induced apoptosis in these cancer cells. However, HECTD3 over-expression leads to a decreased cisplatin-induced apoptosis, whereas overexpression of MALT1 partially rescues HECTD3 depletion-induced apoptosis. These findings suggest that HECTD3 promotes cell survival through stabilizing MALT1. Our data have important implications in cancer therapy by providing novel molecular targets.

Indexed as

Amino Acid SequenceApoptosisCaspasesCell Line, TumorCell SurvivalCisplatinDrug Resistance, NeoplasmHEK293 CellsHeLa CellsHumansMCF-7 CellsMolecular Sequence DataMucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 ProteinNeoplasm ProteinsUbiquitinationUbiquitin-Protein LigasesCaspasesCisplatinHECTD3 protein, humanMALT1 protein, humanMucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 ProteinNeoplasm ProteinsUbiquitin-Protein Ligases

Identifiers

PMID23358872
PMCPMC3556937
OpenAlexW1604788582

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.