Evidence map›Paper›PMID 35729325›Full record

ArticleExperimental & molecular medicine2022

The CDK1/TFCP2L1/ID2 cascade offers a novel combination therapy strategy in a preclinical model of bladder cancer.

Jinbeom Heo, Jinyoung Lee, Yun Ji Nam, YongHwan Kim, HongDuck Yun, Seungun Lee, Hyein Ju, Chae-Min Ryu, Seon Min Jeong, Jinwon Lee and 6 more

Open access · goldAbstract read
In one paragraph

Article in Experimental & molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

25 citing papers in PubMed, 30 citations in OpenAlex.

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  8. Tfcp2l1 as a central integrator of hypoxia, dedifferentiation, and tumor progression.Journal of experimental & clinical cancer research : CR · 2025
    Review
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  14. Bioactive materials · 2024
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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

16 authors at 2 institutions in 1 country.

Jinbeom Heo *Department of Biomedical Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
Jinyoung Lee *Department of Biomedical Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
Yun Ji Nam *Department of Biomedical Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
YongHwan KimDepartment of Biomedical Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
HongDuck YunDepartment of Biomedical Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
Seungun LeeDepartment of Biomedical Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
Hyein JuDepartment of Biomedical Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
Chae-Min RyuDepartment of Biomedical Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
Seon Min JeongDepartment of Biomedical Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
Jinwon LeeDepartment of Biomedical Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
Jisun LimDepartment of Biomedical Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
Yong Mee ChoDepartment of Pathology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
Eui Man JeongDepartment of Pharmacy, College of Pharmacy, Jeju National University, Jeju, Korea.ORCID http://orcid.org/0000-0003-0692-2033
Bumsik HongDepartment of Urology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea. bshong@amc.seoul.kr.
Jaekyoung SonDepartment of Biomedical Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea. jaekson@amc.seoul.kr.
Dong-Myung ShinDepartment of Biomedical Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea. d0shin03@amc.seoul.kr.ORCID http://orcid.org/0000-0002-0511-5750
Ulsan College · KRJeju National University · KR

Funding

CAPACITY BUILDING ASSISTANCE TO STRENGTHEN PUBLIC HEALTH IMMUNIZATION INFRASTRUCTURE AND PERFORMANCEU38IP000871 · IP · WEST VIRGINIA STATE DEPT HLTH/HUMAN RSCS · PI HADDY, LORETTA · 2015 to 2015
$2.0M
Factors Associated with Uptake of Immunization StandardsU01IP000033 · IP · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI FONTANESI, JOHN MARTIN · 2004 to 2005
–
Improving Influenza Vaccinations of Nursing Home StaffU01IP000035 · IP · PUBLIC HEALTH FOUNDATION ENTERPRISES · PI KIMURA, AKIKO C · 2004 to 2005
–
NCIRD CDC HHS U01 IP000033NCIRD CDC HHS U01 IP000035NCIRD CDC HHS U38 IP000871
6 · The paper itself

Abstract

Aberrant activation of embryogenesis-related molecular programs in urothelial bladder cancer (BC) is associated with stemness features related to oncogenic dedifferentiation and tumor metastasis. Recently, we reported that overexpression of transcription factor CP2-like protein-1 (TFCP2L1) and its phosphorylation at Thr177 by cyclin-dependent kinase-1 (CDK1) play key roles in regulating bladder carcinogenesis. However, the clinical relevance and therapeutic potential of this novel CDK1-TFCP2L1 molecular network remain elusive. Here, we demonstrated that inhibitor of DNA binding-2 (ID2) functions as a crucial mediator by acting as a direct repressive target of TFCP2L1 to modulate the stemness features and survival of BC cells. Low ID2 and high CDK1 expression were significantly associated with unfavorable clinical characteristics. TFCP2L1 downregulated ID2 by directly binding to its promoter region. Consistent with these findings, ectopic expression of ID2 or treatment with apigenin, a chemical activator of ID2, triggered apoptosis and impaired the proliferation, suppressed the stemness features, and reduced the invasive capacity of BC cells. Combination treatment with the specific CDK1 inhibitor RO-3306 and apigenin significantly suppressed tumor growth in an orthotopic BC xenograft animal model. This study demonstrates the biological role and clinical utility of ID2 as a direct target of the CDK1-TFCP2L1 pathway for modulating the stemness features of BC cells.

Indexed as

Antineoplastic Combined Chemotherapy ProtocolsCDC2 Protein KinaseInhibitor of Differentiation Protein 2Repressor ProteinsUrinary Bladder NeoplasmsAnimalsApigeninApoptosisCell ProliferationCyclin-Dependent KinasesHumansQuinolinesThiazolesTranscription FactorsXenograft Model Antitumor AssaysApigeninCDC2 Protein KinaseCDK1 protein, humanCyclin-Dependent KinasesID2 protein, humanInhibitor of Differentiation Protein 2QuinolinesRepressor ProteinsRO 3306TFCP2L1 protein, humanThiazolesTranscription Factors

Identifiers

PMID35729325
PMCPMC9256744
OpenAlexW4283315148

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.