Evidence map›Paper›PMID 34369850›Full record

ArticleCell cycle (Georgetown, Tex.)2021

DTYMK promote hepatocellular carcinoma proliferation by regulating cell cycle.

Tianhao Zhou, Rui Qin, Susu Shi, Hua Zhang, Chuanling Niu, Gaoda Ju, Sen Miao

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

17 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Sulfide regulation and catabolism in health and disease.Signal transduction and targeted therapy · 2025
    Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. The evolving landscape of involvement of DTYMK enzymes in cancer.Medical oncology (Northwood, London, England) · 2023
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
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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

7 authors at 4 institutions in 1 country.

Tianhao ZhouKey Laboratory of Breast Cancer Prevention and Treatment of the Ministry of Education, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center of Cancer, Tianjin, China.
Rui QinDepartment of Pathology, Affiliated Hospital of Jining Medical University, Jining, China.
Susu ShiDepartment of Oncology, Beijing Cancer Hospital, Peking University, Beijing, China.
Hua ZhangDepartment of Pathology, Affiliated Hospital of Jining Medical University, Jining, China.
Chuanling NiuDepartment of Pathology, Affiliated Hospital of Jining Medical University, Jining, China.
Gaoda JuDepartment of Oncology, Beijing Cancer Hospital, Peking University, Beijing, China.
Sen MiaoDepartment of Pathology, Affiliated Hospital of Jining Medical University, Jining, China.
Affiliated Hospital of Jining Medical University · CNPeking University · CNPeking University Cancer Hospital · CNShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Overexpression of DTYMK is related with tumorigenesis and progression in several human tumors. However, the role of upregulated DTYMK in hepatocellular carcinoma (HCC) patients still remains unclear. In this study, the DTYMK expression in HCC tumors was evaluated in three GEO series (GSE14520, GSE54236, GSE63898), TCGA-LIHC, and ICGC-IRLR-JP cohorts. Survival analysis of DTYMK based on TCGA-LIHC and ICGC-LIRI-JP cohorts was conducted. We found that DTYMK was dramatically upregulated in tumor tissue compared with that in adjacent liver tissue. Kaplan-Meier analysis revealed that high expression of DTYMK in HCC patients' tumor tissue was significantly corresponded to worse overall survival (OS) (P < 0.05). Further analysis showed that overexpressing DTYMK led to poor relapse free survival (RFS) and disease-specific survival (DSS) (all P < 0.05). In conclusion, DTYMK is upregulated in tumors and correlated with poor prognosis in HCC patients. In our report, DTYMK is higher expression in HCC cancer tissue and cell line than tumor adjacent tissue and normal liver cell line. Knocking down DTYMK can inhabit tumor cell proliferation by interfering cell cycle, whereas overexpression of DTYMK can promote tumor cell proliferation. These findings indicate that upregulation of DTYMK enhances tumor growth and proliferation by promoting cell cycle.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsBiomarkers, TumorCell CycleCell ProliferationGene Expression Regulation, NeoplasticHumansKaplan-Meier EstimateBiomarkers, Tumorcell cyclecell proliferationDTYMKhepatocarcinoma

Identifiers

PMID34369850
PMCPMC8489954
OpenAlexW3189743554

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.