Evidence map›Paper›PMID 36096885›Full record

ArticleCell death & disease2022

E2F1/CKS2/PTEN signaling axis regulates malignant phenotypes in pediatric retinoblastoma.

Meng Chen, Zhaozhao Zhao, Lianqun Wu, Jiancheng Huang, Peng Yu, Jiang Qian, Ting Ni, Chen Zhao

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

14 citing papers in PubMed, 19 citations in OpenAlex.

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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

8 authors at 2 institutions in 1 country.

Meng Chen *Eye Institute, Eye & ENT Hospital, Shanghai Medical College, Fudan University, Shanghai, China.
Zhaozhao Zhao *State Key Laboratory of Genetic Engineering, Collaborative Innovation Center of Genetics and Development, Human Phenome Institute, School of Life Sciences, Fudan University, Shanghai, China.
Lianqun Wu *Eye Institute, Eye & ENT Hospital, Shanghai Medical College, Fudan University, Shanghai, China.
Jiancheng Huang *Eye Institute, Eye & ENT Hospital, Shanghai Medical College, Fudan University, Shanghai, China.
Peng YuState Key Laboratory of Genetic Engineering, Collaborative Innovation Center of Genetics and Development, Human Phenome Institute, School of Life Sciences, Fudan University, Shanghai, China.
Jiang QianEye Institute, Eye & ENT Hospital, Shanghai Medical College, Fudan University, Shanghai, China. qianjiang58@vip.126.com.
Ting NiState Key Laboratory of Genetic Engineering, Collaborative Innovation Center of Genetics and Development, Human Phenome Institute, School of Life Sciences, Fudan University, Shanghai, China. tingni@fudan.edu.cn.
Chen ZhaoEye Institute, Eye & ENT Hospital, Shanghai Medical College, Fudan University, Shanghai, China. dr_zhaochen@163.com.ORCID 0000-0003-1373-7637
Chinese Academy of Medical Sciences & Peking Union Medical College · CNFudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Retinoblastoma (RB) is the most common pediatric intraocular malignancy and is a serious vision- and life-threatening disease. The biallelic mutation of the retinoblastoma gene RB1 is the initial event in the malignant transformation of RB, but the exact molecular mechanism is still unclear. E2F transcription factors can be activated by RB1 loss of function and lead to uncontrolled cell division. Among E2F family numbers, E2F1 has higher expression abundance than E2F2 and E2F3 in RB clinical samples. By integrating E2F1 ChIP-seq data, RNA-seq profiling from RB samples and RNA-seq profiling upon E2F1 knockdown, together with pathway analysis, literature searching and experimental validation, we identified Cyclin-dependent kinases regulatory subunit 2 (CKS2) as a novel regulator in regulating tumor-associated phenotypes in RB. CKS2 exhibited aberrantly higher expression in RB. Depletion of CKS2 in Y79 retinoblastoma cell line led to reduced cell proliferation, delayed DNA replication and decreased clonogenic growth. Downregulation of CKS2 also slowed tumor xenograft growth in nude mice. Importantly, reversed expression of CKS2 rescued cancer-associated phenotypes. Mechanistically, transcription factor E2F1 enhanced CKS2 expression through binding to its promoter and CKS2 regulated the cancer-associated PI3K-AKT pathway. This study discovered E2F1/CKS2/PTEN signaling axis regulates malignant phenotypes in pediatric retinoblastoma, and CKS2 may serve as a potential therapeutic target for this disease.

Indexed as

CDC2-CDC28 KinasesRetinal NeoplasmsRetinoblastomaAnimalsCell Cycle ProteinsE2F1 Transcription FactorHumansMiceMice, NudePhenotypePhosphatidylinositol 3-KinasesPTEN PhosphohydrolaseCDC2-CDC28 KinasesCell Cycle ProteinsCKS2 protein, humanE2F1 protein, humanE2F1 Transcription FactorPhosphatidylinositol 3-KinasesPTEN PhosphohydrolasePTEN protein, human

Identifiers

PMID36096885
PMCPMC9468144
OpenAlexW4295269421

What OpenQuestion holds

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LicenceCC BY
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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.