Evidence map›Paper›PMID 38880876›Full record

ArticleBiology direct2024

The deubiquitinating protein OTUD6B promotes lung adenocarcinoma progression by stabilizing RIPK1.

Miaomiao Yang, Yujie Wei, Xin He, Changwei Xia

Abstract read
In one paragraph

Article in Biology direct, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–field-weighted citation impact
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

11 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. OTU deubiquitinases in disease: roles and targeting.Trends in molecular medicine · 2026
    Review
  5. Review
  6. Targeting RIPK1 to modulate cell death and tumour microenvironment in cancer therapy.Journal of enzyme inhibition and medicinal chemistry · 2025
    Review
  7. Article
  8. ATRA upregulates OTUD6B to recruit CD8Cell death & disease · 2025
    Article
  9. Article
  10. Article
  11. 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.

Miaomiao Yang *Department of Nephrology, Henan Provincial Key Laboratory of Kidney Disease and Immunology, Henan Provincial Clinical Research Center for Kidney Disease, Henan Provincial People's Hospital and People's Hospital of Zhengzhou University, 7 Weiwu Road, Zhengzhou, 450053, Henan, China. 15736738997@163.com.
Yujie Wei *National Engineering Laboratory for Internet Medical Systems and Applications, The First Affiliated Hospital of Zhengzhou University, Zhengzhou University, No. 1 Jianshe Road, Erqi District, Zhengzhou, 450052, Henan, China.
Xin HeDepartment of Clinical Laboratory, The Fifth Affiliated Hospital of Zhengzhou University, No.3 Kangfuqian Street, Erqi District, Zhengzhou, China.
Changwei XiaHeart Center of Henan Provincial People's Hospital, Central China Fuwai Hospital of Zhengzhou University, Fuwai Central China Cardiovascular Hospital and Central China Branch of National Center Fuwai Cardiovascular Diseases, Zhengzhou, China. 13523542638@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThere is growing evidence indicating that deubiquitinating enzymes may contribute to tumor progression and can serve as promising therapeutic targets.

methodsThe overexpression of deubiquitinase OTUD6B in lung adenocarcinoma (LUAD) and its adjacent tissues was analyzed by immunohistochemistry and TCGA/GO database. Survival analysis further supported OTUD6B as a potential target for LUAD treatment. We assessed the effect of OTUD6B on LUAD cell growth using cell viability assays and conducted TUNEL staining, migration, and invasion experiments to investigate the impact of OTUD6B on the apoptosis and metastasis of LUAD cells. Additionally, we established a transplanted tumor model in nude mice to validate our findings in vivo. Finally, using IP mass spectrometry and co-IP experiments, we screened and confirmed the influence of RIPK1 as a substrate of OTUD6B in LUAD.

resultsOTUD6B is highly overexpressed in human LUAD and predicts poor prognosis in LUAD patients. OTUD6B knockdown inhibited the proliferation of LUAD cells and enhanced apoptosis and inhibited metastasis in LUAD cells suppressed. A549 xenografts revealed that OTUD6B deletion can slow down tumour growth. Additionally, OTUD6B can bind to RIPK1, reduce its ubiquitination level and increase its protein stability.

conclusionsOur results suggest that OTUD6B is a promising clinical target for LUAD treatment and that targeting OTUD6B may constitute an effective anti-LUAD strategy.

Indexed as

Adenocarcinoma of LungLung NeoplasmsReceptor-Interacting Protein Serine-Threonine KinasesA549 CellsAnimalsApoptosisCell Line, TumorCell ProliferationDeubiquitinating EnzymesDisease ProgressionEndopeptidasesHumansMiceMice, NudeProtein StabilityUbiquitinationDeubiquitinating EnzymesEndopeptidasesOTUD6B protein, humanReceptor-Interacting Protein Serine-Threonine KinasesRIPK1 protein, humanDeubiquitinating proteinLung adenocarcinomaOTUD6BRIPK1Tumor progression

Identifiers

PMID38880876
PMCPMC11181667

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.