Evidence map›Paper›PMID 39366214›Full record

ArticleNeoplasia (New York, N.Y.)2024

Prenatal p25-activated Cdk5 induces pituitary tumorigenesis through MCM2 phosphorylation-mediated cell proliferation.

Yingwei Huang, Qiqi Wang, Weiwei Zhou, Yawei Jiang, Kai He, Wei Huang, Yating Feng, Hong Wu, Lijuan Liu, Yue Pan and 14 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neoplasia (New York, N.Y.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Review
  5. 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

24 authors.

Yingwei HuangDepartment of Neurology, Nanfang Hospital, Southern Medical University, Guangzhou, China; Department of Neurology, Jiangmen Central Hospital, Jiangmen, China.
Qiqi WangDepartment of Neurology, Nanfang Hospital, Southern Medical University, Guangzhou, China; Department of Neurology, The First Affiliated Hospital of Gannan Medical University, Ganzhou, China.
Weiwei ZhouDepartment of Biochemistry, School of Medicine, Southern University of Science and Technology, Shenzhen, China.
Yawei JiangDepartment of Neurology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Kai HeDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, and Guangdong Provincial Key Laboratory of Single Cell Technology and Application, Southern Medical University, Guangzhou, China.
Wei HuangDepartment of Neurology, the First People's Hospital of Shunde, Southern Medical University, Guangzhou, China.
Yating FengDepartment of Biochemistry, School of Medicine, Southern University of Science and Technology, Shenzhen, China.
Hong WuDepartment of Neurology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Lijuan LiuDepartment of Biochemistry, School of Medicine, Southern University of Science and Technology, Shenzhen, China.
Yue PanDepartment of Neurology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Yihua HuangDepartment of Neurology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Zirui ChenDepartment of Neurology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Wei LiDepartment of Neurology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Yaowei HuangDepartment of Neurology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Guanchuan LinDepartment of Biochemistry, School of Medicine, Southern University of Science and Technology, Shenzhen, China.
Yulong ZhangDepartment of Biochemistry, School of Medicine, Southern University of Science and Technology, Shenzhen, China.
Yongyan RenCentral Laboratory, Southern Medical University, Guangzhou, China.
Kaibiao XuDepartment of Neurology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Yanlin YuLaboratory of Cancer Biology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD, United States.
Yuping PengDepartment of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Xinghua PanDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, and Guangdong Provincial Key Laboratory of Single Cell Technology and Application, Southern Medical University, Guangzhou, China; Precision Regenerative Medicine Research Centre, Medical Science Division, and State Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Macao, China; China Ministry Education Key Laboratory of Infectious Diseases Research in South China, Southern Medical University, Guangzhou, China. Electronic address: panxinghua@must.edu.mo.
Suyue PanDepartment of Neurology, Nanfang Hospital, Southern Medical University, Guangzhou, China. Electronic address: pansuyue@smu.edu.cn.
Hailiang HuDepartment of Biochemistry, School of Medicine, Southern University of Science and Technology, Shenzhen, China. Electronic address: huhl@sustech.edu.cn.
Yafang HuDepartment of Neurology, Nanfang Hospital, Southern Medical University, Guangzhou, China. Electronic address: yafanghu@smu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aberrant expression of cyclin-dependent kinase 5 (Cdk5) has been reported in pituitary adenomas. However, the role of Cdk5 in the tumorigenesis remains unclear. We show that prenatal p25-activated Cdk5 phosphorylates minichromosome maintenance protein 2 (Mcm2), enhancing minichromosome maintenance (MCM) family proteins and driving intermediate lobe-located melanotrope-originated pituitary tumorigenesis. In a mouse model with CaMKII promoter-driven transgenic induction of p25, we observed intermediate lobe-originated pituitary adenoma producing non-functional proopiomelanocortin (POMC)-derived peptides under persistent p25 overexpression. Single-cell RNA sequencing revealed Mcm2 may play an important role during tumor progression. Subsequently, Mcm2 was identified as a potential phosphorylated substrate of Cdk5, mediating the tumorous proliferation of melanotrope cells. Silencing Cdk5 or Mcm2 suppressed cell proliferation and colony formation in the 293T cell lines. Therefore, our findings provide a new mouse model of intermediate lobe-originated pituitary adenoma induced by p25/Cdk5 and unveil a previously unappreciated role of Cdk5 and Mcm2 in pituitary adenoma tumorigenesis.

Indexed as

Cell ProliferationCyclin-Dependent Kinase 5Minichromosome Maintenance Complex Component 2Pituitary NeoplasmsAdenomaAnimalsCarcinogenesisCell Transformation, NeoplasticDisease Models, AnimalHumansMiceMice, TransgenicPhosphorylationCyclin-Dependent Kinase 5Minichromosome Maintenance Complex Component 2Cdk5Mcm2p25Pituitary adenomaSingle-cell sequencing

Identifiers

PMID39366214
PMCPMC11489071

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

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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.