Evidence map›Paper›PMID 29266545›Full record

ArticleCell proliferation2018

Thymidine kinase 1 silencing retards proliferative activity of pancreatic cancer cell via E2F1-TK1-P21 axis.

Xiaole Zhu, Chenyuan Shi, Yunpeng Peng, Lingdi Yin, Min Tu, Qiuyang Chen, Chaoqun Hou, Qiang Li, Yi Miao

Open access · bronzeAbstract read
In one paragraph

Article in Cell proliferation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.8field-weighted citation impact, top 13% 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

24 citing papers in PubMed, 43 citations in OpenAlex.

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  7. mCell death & disease · 2023
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  14. NF-Journal of oncology · 2022
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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

9 authors at 1 institution in 1 country.

Xiaole ZhuPancreas Center, First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu Province, China.
Chenyuan ShiPancreas Center, First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu Province, China.
Yunpeng PengPancreas Center, First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu Province, China.
Lingdi YinPancreas Center, First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu Province, China.
Min TuPancreas Center, First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu Province, China.
Qiuyang ChenPancreas Center, First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu Province, China.
Chaoqun HouPancreas Center, First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu Province, China.
Qiang LiPancreas Center, First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu Province, China.ORCID http://orcid.org/0000-0001-5129-2603
Yi MiaoPancreas Center, First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu Province, China.
Jiangsu Province Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesThymidine kinase 1 (TK1) is one of the salvage enzymes engaged in the synthesis of DNA. Although a pro-carcinogenetic role of TK1 has been reported in various types of cancers, its role in pancreatic ductal adenocarcinoma (PDAC) is still unknown. The study is aimed to elaborate the function of TK1 in PDAC and the potential mechanisms in the following study. MATERIALS AND

methodsTK1 expression was analysed by immunohistochemistry, real-time PCR and Western blot, and its relationship with clinicopathological characteristics of PDAC patients was further investigated. To verify the function of TK1 and potential mechanism, TK1 siRNA was used to transfect PDAC cells and performed a series of assays in cell and animal models.

resultsThe level of TK1 expression was higher in cancerous tissues compared with matched adjacent tissues. TK1 overexpression was associated with progression of PDAC and poor prognosis. Knockdown of TK1 could suppress cell proliferation via inducing S phase arrest mediated by upregulation of P21. Further mechanism investigation suggested that transcription factor E2F-1 could directly regulate the TK1 and promote tumour proliferation.

conclusionsThe results suggested that TK1 might be involved in the development and progression of PDAC by regulating cell proliferation and show that TK1 may work as a promising therapeutic target in patients with PDAC.

Indexed as

Cell ProliferationAgedAnimalsApoptosisCarcinoma, Pancreatic DuctalCell Line, TumorCell MovementCyclin-Dependent Kinase Inhibitor p21Disease ProgressionE2F1 Transcription FactorFemaleGene ExpressionGene Knockdown TechniquesHumansMaleMice, Inbred BALB CCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21E2F1 protein, humanE2F1 Transcription FactorRNA, Small InterferingThymidine Kinasethymidine kinase 1

Identifiers

PMID29266545
PMCPMC6528927
OpenAlexW2780127421

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.