Evidence map›Paper›PMID 37744402›Full record

ArticleJournal of bioinformatics and systems biology : Open access2023

CDKs Functional Analysis in Low Proliferating Early-Stage Pancreatic Ductal Adenocarcinoma.

Shikai Zhu, Huining Yang, Lingling Liu, Zhilin Jiang, Juanjuan Ji, Xiao Wang, Lin Zhong, Fulin Liu, Xueliang Gao, Haizhen Wang and 1 more

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of bioinformatics and systems biology : Open access, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.2field-weighted citation impact, top 32% 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

0 citing papers in PubMed, 1 citations in OpenAlex.

No citing paper in PubMed yet.

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

11 authors at 2 institutions in 1 country.

Shikai ZhuSichuan Provincial Key Laboratory for Human Disease Gene Study, Department of Laboratory Medicine, Center for Medical Genetics, Sichuan Provincial People's Hospital, School of Medicine,University of Electronic Science and Technology of China, Chengdu, China.
Huining YangSichuan Provincial Key Laboratory for Human Disease Gene Study, Department of Laboratory Medicine, Center for Medical Genetics, Sichuan Provincial People's Hospital, School of Medicine,University of Electronic Science and Technology of China, Chengdu, China.
Lingling LiuDepartment of Cell and Molecular Pharmacology & Experimental Therapeutics.
Zhilin JiangSichuan Provincial Key Laboratory for Human Disease Gene Study, Department of Laboratory Medicine, Center for Medical Genetics, Sichuan Provincial People's Hospital, School of Medicine,University of Electronic Science and Technology of China, Chengdu, China.
Juanjuan JiSichuan Provincial Key Laboratory for Human Disease Gene Study, Department of Laboratory Medicine, Center for Medical Genetics, Sichuan Provincial People's Hospital, School of Medicine,University of Electronic Science and Technology of China, Chengdu, China.
Xiao WangSichuan Provincial Key Laboratory for Human Disease Gene Study, Department of Laboratory Medicine, Center for Medical Genetics, Sichuan Provincial People's Hospital, School of Medicine,University of Electronic Science and Technology of China, Chengdu, China.
Lin ZhongSichuan Provincial Key Laboratory for Human Disease Gene Study, Department of Laboratory Medicine, Center for Medical Genetics, Sichuan Provincial People's Hospital, School of Medicine,University of Electronic Science and Technology of China, Chengdu, China.
Fulin LiuSichuan Provincial Key Laboratory for Human Disease Gene Study, Department of Laboratory Medicine, Center for Medical Genetics, Sichuan Provincial People's Hospital, School of Medicine,University of Electronic Science and Technology of China, Chengdu, China.
Xueliang GaoDepartment of Cell and Molecular Pharmacology & Experimental Therapeutics.
Haizhen WangDepartment of Cell and Molecular Pharmacology & Experimental Therapeutics.
Yu ZhouSichuan Provincial Key Laboratory for Human Disease Gene Study, Department of Laboratory Medicine, Center for Medical Genetics, Sichuan Provincial People's Hospital, School of Medicine,University of Electronic Science and Technology of China, Chengdu, China.
Medical University of South Carolina · USMUSC Hollings Cancer Center · US

Funding

The role of SMAD1 and SATB2 in colon patterningP20GM130457 · NIGMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI Evan R Delgado · 2020 to 2026
$18.7M
Novel functions of CDK6 in T-cell leukemia progressionR37CA251165 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI Haizhen Wang · 2021 to 2026
$2.0M
NCI NIH HHS R37 CA251165NIGMS NIH HHS P20 GM130457
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is a highly devastating disease with a poor prognosis and growing incidence. In this study, we explored the potential roles of CDK1, CDK2, CDK4, and CDK6 in the progression of early-stage PDAC. Clinicopathologic and mRNA expression data and treatment information of 140 patients identified with stage I/II PDAC who underwent pancreaticoduodenectomy were obtained from the Cancer Genome Atlas data set. Our bioinformatic analysis showed that higher CDK1, CDK2, CDK4, or CDK6 expression was associated with a shorter median survival of the early-stage PDAC patients. Of note, in the low-proliferating pancreatic cancer group, CDKs expressions were significantly associated with proteins functioning in apoptosis, metastasis, immunity, or stemness. Among the low-proliferating PDAC, higher expression of CDK1 was associated with the shorter survival of patients, suggesting that CDK1 may regulate PDAC progression through cell cycle-independent mechanisms. Our experimental data showed that CDK1 knockdown/inhibition significantly suppressed the expression levels of AHR and POU5F1, two critical proteins functioning in cancer cell metastasis and stemness, in low-proliferating, but not in high-proliferating pancreatic cancer cells. In all, our study suggests that CDKs regulate PDAC progression not only through cell proliferation but also through apoptosis, metastasis, immunity, and stemness.

Indexed as

ApoptosisCyclin-dependent kinaseEarly stageImmunogenicityLow-proliferating cancer cellsMetastasisPancreatic ductal adenocarcinoma (PDAC)Survival

Identifiers

PMID37744402
PMCPMC10516534
OpenAlexW4385957746

What OpenQuestion holds

Textmetadata
LicenceTDM
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.