Evidence map›Paper›PMID 39087955›Full record

ArticleCancer biology & therapy2024

Autophagic degradation of CDK4 is responsible for G0/G1 cell cycle arrest in NVP-BEZ235-treated neuroblastoma.

Zhen Liu, Xiao-Yang Wang, Han-Wei Wang, Shan-Ling Liu, Chao Zhang, Feng Liu, Ying Guo, Feng-Hou Gao

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PubMed Full text at PMC Publisher
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Article in Cancer biology & therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

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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

2 citing papers in PubMed.

  1. Article
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4 · The record

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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

8 authors.

Zhen LiuDepartment of Clinical Laboratory, Shanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai, China.
Xiao-Yang WangDepartment of Blood Transfusion, The Sanmenxia Central Hospital, Sanmenxia, Henan Province, China.
Han-Wei WangDepartment of Rheumatology and Immunology, Bengbu Third People's Hospital Affiliated to Bengbu Medical College, Bengbu, Anhui, China.
Shan-Ling LiuDepartment of Clinical Laboratory, The First Hospital of Changsha City,Changsha, Hunan, China.
Chao ZhangDepartment of Geriatrics, Shanghai ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Feng LiuDepartment of Oncology, Shanghai ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Ying GuoDepartment of Pathology, Yellow River Hospital Attached Henan University of Science and Technology, Sanmenxia, Henan Province, China.
Feng-Hou GaoDepartment of Oncology, Shanghai ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0000-0001-5032-6955

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCDK4 is highly expressed and associated with poor prognosis and decreased survival in advanced neuroblastoma (NB). Targeting CDK4 degradation presents a potentially promising therapeutic strategy compared to conventional CDK4 inhibitors. However, the autophagic degradation of the CDK4 protein and its anti-proliferation effect in NB cells has not been mentioned.

resultsWe identified autophagy as a new pathway for the degradation of CDK4. Firstly, autophagic degradation of CDK4 is critical for NVP-BEZ235-induced G0/G1 arrest, as demonstrated by the overexpression of CDK4, autophagy inhibition, and blockade of autophagy-related genes. Secondly, we present the first evidence that p62 binds to CDK4 and then enters the autophagy-lysosome to degrade CDK4 in a CTSB-dependent manner in NVP-BEZ235 treated NB cells. Similar results regarding the interaction between p62 and CDK4 were observed in the NVP-BEZ235 treated NB xenograft mouse model.

conclusionsAutophagic degradation of CDK4 plays a pivotal role in G0/G1 cell cycle arrest in NB cells treated with NVP-BEZ235.

Indexed as

AutophagyCyclin-Dependent Kinase 4G1 Phase Cell Cycle CheckpointsNeuroblastomaAnimalsCell Line, TumorCell ProliferationHumansImidazolesMiceMice, NudeProteolysisQuinolinesResting Phase, Cell CycleXenograft Model Antitumor AssaysCDK4 protein, humanCyclin-Dependent Kinase 4ImidazolesQuinolinesautophagic degradationCDK4neuroblastomaNVP-BEZ235P62

Identifiers

PMID39087955
PMCPMC11296530

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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.