Evidence map›Paper›PMID 38309745›Full record

ArticleSaudi medical journal2024

CKS1B as a potential target for prognostic assessment and intervention in pancreatic cancer and its role in abnormal proliferation and cellular phenotype through mediation of cell cycle signaling pathways.

Yuzhu Tang, Xiaohua Lan, Maohui Yan, Zhiguang Fu, Hongqi Li

Open access · diamondAbstract read
In one paragraph

Article in Saudi medical journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.1field-weighted citation impact, top 21% 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

3 citing papers in PubMed, 4 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

5 authors at 1 institution in 1 country.

Yuzhu TangFrom the Department of specialty (Yuzhu, Xiaohua), Graduate School of Hebei North University, Zhangjiakou, and from the Department of Radiation Oncology (Yuzhu, Maohui, Zhiguang, Hongqi), Air Force Medical Center, PLA, Beijing, China.
Xiaohua LanFrom the Department of specialty (Yuzhu, Xiaohua), Graduate School of Hebei North University, Zhangjiakou, and from the Department of Radiation Oncology (Yuzhu, Maohui, Zhiguang, Hongqi), Air Force Medical Center, PLA, Beijing, China.
Maohui YanFrom the Department of specialty (Yuzhu, Xiaohua), Graduate School of Hebei North University, Zhangjiakou, and from the Department of Radiation Oncology (Yuzhu, Maohui, Zhiguang, Hongqi), Air Force Medical Center, PLA, Beijing, China.
Zhiguang FuFrom the Department of specialty (Yuzhu, Xiaohua), Graduate School of Hebei North University, Zhangjiakou, and from the Department of Radiation Oncology (Yuzhu, Maohui, Zhiguang, Hongqi), Air Force Medical Center, PLA, Beijing, China.
Hongqi LiFrom the Department of specialty (Yuzhu, Xiaohua), Graduate School of Hebei North University, Zhangjiakou, and from the Department of Radiation Oncology (Yuzhu, Maohui, Zhiguang, Hongqi), Air Force Medical Center, PLA, Beijing, China.ORCID https://orcid.org/0000-0001-6944-701X
Hebei North University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesTo investigate the role of cell cycle protein-dependent kinase regulatory subunit 1B (CKS1B) in driving the aggressive and rapid proliferation observed in pancreatic cancer.

methodsA comprehensive analysis was carried out using raw mRNA information and data from 2 databases: the cancer genome atlas and gene expression omnibus. The differential expression of CKS1B at the mRNA and tissue levels in cancer and adjacent paracancerous tissues were assessed. Additionally, the relationship of CKS1B expression and overall survival (OS) rate was investigated using Kaplan-Meier survival curves. Potential molecular mechanisms by which CKS1B may influence the biological characteristics of pancreatic cancer were explored using resources available within the encyclopedia of RNA interactomes database.

resultsThe CKS1B exhibited significant differential expression at the mRNA as well as protein levels. A correlation with statistical significance between CKS1B expression and N stage, age, and alcohol consumption was observed. Notably, high CKS1B expression was determined as a predictive factor for worse OS. Furthermore, the analysis revealed a potential synergistic role between CKS1B and the molecule PKMYT1, which could impact the ATR-Chk1-Cdc25 signaling pathway and disrupt the G2/M checkpoint within the cell cycle, ultimately promoting abnormal tumor proliferation.

conclusionThe CKS1B may serve as a novel potential prognostic factor in pancreatic cancer and is involved in the abnormal proliferation biology phenotype by mediating cell cycle signaling pathways.

Indexed as

CDC2-CDC28 KinasesPancreatic NeoplasmsCell CycleCell ProliferationHumansMembrane ProteinsPhenotypePrognosisProtein Serine-Threonine KinasesProtein-Tyrosine KinasesRNA, MessengerSignal TransductionCDC2-CDC28 KinasesCKS1B protein, humanMembrane ProteinsPKMYT1 protein, humanProtein Serine-Threonine KinasesProtein-Tyrosine KinasesRNA, MessengermicroRNAspancreatic cancerPKMYT1regulatory subunit 1B

Identifiers

PMID38309745
PMCPMC11115417
OpenAlexW4391511488

What OpenQuestion holds

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LicenceCC BY-NC
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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.