Evidence map›Paper›PMID 31685992›Full record

ArticleNature cell biology2019

PTENα and PTENβ promote carcinogenesis through WDR5 and H3K4 trimethylation.

Shao-Ming Shen, Cheng Zhang, Meng-Kai Ge, Shuang-Shu Dong, Li Xia, Ping He, Na Zhang, Yan Ji, Shuo Yang, Yun Yu and 4 more

Erratum issuedAbstract read
PubMed Publisher
In one paragraph

Article in Nature cell biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

43 citing papers in PubMed, 86 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 2 institutions in 1 country.

Shao-Ming Shen *Department of Pathophysiology, State Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Ren-Ji Hospital and Key Laboratory of Cell Differentiation and Apoptosis of the Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China. smshen@shsmu.edu.cn.ORCID http://orcid.org/0000-0001-8334-9790
Cheng Zhang *Department of Pathophysiology, State Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Ren-Ji Hospital and Key Laboratory of Cell Differentiation and Apoptosis of the Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Meng-Kai Ge *Department of Pathophysiology, State Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Ren-Ji Hospital and Key Laboratory of Cell Differentiation and Apoptosis of the Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Shuang-Shu Dong *Shanghai Institute of Nutrition and Health, Shanghai Institutes for Biological Sciences, University of the Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, China.
Li XiaDepartment of Pathophysiology, State Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Ren-Ji Hospital and Key Laboratory of Cell Differentiation and Apoptosis of the Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Ping HeDepartment of Pathophysiology, State Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Ren-Ji Hospital and Key Laboratory of Cell Differentiation and Apoptosis of the Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Na ZhangDepartment of Pathophysiology, State Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Ren-Ji Hospital and Key Laboratory of Cell Differentiation and Apoptosis of the Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yan JiShanghai Institute of Nutrition and Health, Shanghai Institutes for Biological Sciences, University of the Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, China.
Shuo YangDepartment of Pathophysiology, State Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Ren-Ji Hospital and Key Laboratory of Cell Differentiation and Apoptosis of the Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yun YuDepartment of Pathophysiology, State Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Ren-Ji Hospital and Key Laboratory of Cell Differentiation and Apoptosis of the Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Jun-Ke ZhengDepartment of Pathophysiology, State Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Ren-Ji Hospital and Key Laboratory of Cell Differentiation and Apoptosis of the Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Jian-Xiu YuDepartment of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory of Tumor Microenvironment and Inflammation, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Qiang XiaDepartment of Liver Surgery, Ren-Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Guo-Qiang ChenDepartment of Pathophysiology, State Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Ren-Ji Hospital and Key Laboratory of Cell Differentiation and Apoptosis of the Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China. chengq@shsmu.edu.cn.ORCID http://orcid.org/0000-0003-4936-2363
Shanghai Jiao Tong University · CNShanghai Institute of Nutrition and Health · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

PTENα and PTENβ are two longer translational variants of phosphatase and tensin homolog (PTEN) messenger RNA. Their expressional regulations and functions in carcinogenesis remain largely unknown. Here, we demonstrate that, in contrast with the well-established tumour-suppressive role of canonical PTEN, PTENα and PTENβ promote tumourigenesis by directly interacting with the histone H3 lysine 4 (H3K4) presenter WDR5 to promote H3K4 trimethylation and maintain a tumour-promoting signature. We also show that USP9X and FBXW11 bind to the amino-terminal extensions of PTENα/β, and respectively deubiquitinate and ubiquitinate lysines 235 and 239 in PTENα to regulate PTENα/β stability. In accordance, USP9X promotes tumourigenesis and FBXW11 suppresses tumourigenesis through PTENα/β. Taken together, our results indicate that the Pten gene is a double-edged sword for carcinogenesis, and reinterpretation of the importance of the Pten gene in carcinogenesis is warranted.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsbeta-Transducin Repeat-Containing ProteinsCarcinogenesisCarcinoma, HepatocellularCell Line, TumorCell MovementCell ProliferationFemaleHistonesHumansIntracellular Signaling Peptides and ProteinsIsoenzymesLiverLiver NeoplasmsMalebeta-Transducin Repeat-Containing ProteinsFBXW11 protein, humanHistonesIntracellular Signaling Peptides and ProteinsIsoenzymesPTEN PhosphohydrolasePTEN protein, humanUbiquitin-Protein LigasesUbiquitin ThiolesteraseUSP9X protein, humanWDR5 protein, human

Identifiers

PMID31685992
OpenAlexW2984867222

What OpenQuestion holds

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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.