Evidence map›Paper›PMID 41102525›Full record

ArticleScientific reports2025

Identifying TP53RK as a key regulator of colorectal cancer survival and a potential therapeutic target.

Younghee Choi, Seowoo Park, Seojin Yang, Eunju Kim, Youngwon Cho, Hye-Ju Yang, Eugene C Yi, Sang-Hyun Song, Tae-You Kim

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2025. 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

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

2 citing papers in PubMed.

  1. The Role of theLife (Basel, Switzerland) · 2025
    Article
  2. 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

9 authors.

Younghee ChoiDepartment of Molecular Medicine and Biopharmaceutical Sciences, Graduate School of Convergence Science and Technology, Seoul National University, Seoul, 03080, Republic of Korea.
Seowoo ParkDepartment of Molecular Medicine and Biopharmaceutical Sciences, Graduate School of Convergence Science and Technology, Seoul National University, Seoul, 03080, Republic of Korea.
Seojin YangDepartment of Molecular Medicine and Biopharmaceutical Sciences, Graduate School of Convergence Science and Technology, Seoul National University, Seoul, 03080, Republic of Korea.
Eunju KimDepartment of Molecular Medicine and Biopharmaceutical Sciences, Graduate School of Convergence Science and Technology, Seoul National University, Seoul, 03080, Republic of Korea.
Youngwon ChoDepartment of Molecular Medicine and Biopharmaceutical Sciences, Graduate School of Convergence Science and Technology, Seoul National University, Seoul, 03080, Republic of Korea.
Hye-Ju YangDepartment of Molecular Medicine and Biopharmaceutical Sciences, Graduate School of Convergence Science and Technology, Seoul National University, Seoul, 03080, Republic of Korea.
Eugene C YiDepartment of Molecular Medicine and Biopharmaceutical Sciences, Graduate School of Convergence Science and Technology, Seoul National University, Seoul, 03080, Republic of Korea.
Sang-Hyun SongCancer Genomics Research Laboratory, Cancer Research Institute, Seoul National University, Seoul, 03080, Republic of Korea.
Tae-You KimDepartment of Molecular Medicine and Biopharmaceutical Sciences, Graduate School of Convergence Science and Technology, Seoul National University, Seoul, 03080, Republic of Korea. kimty@snu.ac.kr.

Funding

Ministry of Science and ICT, South Korea 2016R1D1A1B03930736
6 · The paper itself

Abstract

Colorectal cancer (CRC) is a leading cause of cancer-related mortality, necessitating the development of novel therapeutic strategies. In the present study, we identified TP53-regulating kinase (TP53RK) as a critical regulator of CRC cell survival and proliferation using a custom clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 library screen targeting serine/threonine kinase-related genes. TP53RK was significantly overexpressed in CRC tissues and was correlated with copy number amplification. Functional validation revealed that TP53RK depletion induced DNA replication stress, apoptosis, and cell cycle arrest, independent from p53 status. Mechanistically, TP53RK stabilized cell division cycle 7 (CDC7), a key kinase regulating DNA replication origin activation, ensuring robust minichromosome maintenance complex protein (MCM) phosphorylation and replication fork progression. Disruption of the TP53RK-CDC7 axis led to reduced MCM2 enrichment at replication origins and impaired DNA replication dynamics. Moreover, TP53RK overexpression sensitized cells to DNA replication stress (aphidicolin) and CDC7 inhibition (XL413), highlighting its potential as a therapeutic strategy. These findings establish TP53RK as a pivotal regulator of DNA replication fidelity and genomic stability, thereby providing a promising therapeutic target for CRC.

Indexed as

Colorectal NeoplasmsProtein Serine-Threonine KinasesApoptosisCell Cycle CheckpointsCell Cycle ProteinsCell Line, TumorCell ProliferationCell SurvivalDNA ReplicationGene Expression Regulation, NeoplasticHCT116 CellsHumansMinichromosome Maintenance Complex Component 2PhosphorylationTumor Suppressor Protein p53CDC7 protein, humanCell Cycle ProteinsMinichromosome Maintenance Complex Component 2Protein Serine-Threonine KinasesTumor Suppressor Protein p53CDC7Colorectal cancerCRISPR/Cas9 screeningDNA replicationTP53RK

Identifiers

PMID41102525
PMCPMC12533122

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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.