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Research ArticleOriginal Article
Open Access

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 and Hongqi Li
Saudi Medical Journal February 2024, 45 (2) 128-138; DOI: https://doi.org/10.15537/smj.2024.45.2.20230132
Yuzhu Tang
From 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.
MM
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Xiaohua Lan
From 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.
MM
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Maohui Yan
From 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.
MD
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Zhiguang Fu
From 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.
MD
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Hongqi Li
From 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.
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  • For correspondence: [email protected]
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    Figure 1

    - Identification of differential genes. A) TCGA pancreatic cancer and paraneoplastic tissues differential genes. B) GEO pancreatic and paraneoplastic tissues differential genes. Green dots indicate a p-value of<0.05 and log2(FC) of >1, while red dots indicate a p-value of <0.05 and log2(FC) of <1. TCGA: the cancer genome atlas, GEO: gene expression omnibus, FC: fold change, FDR: false discovery rate

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    Figure 2

    - Differential expression of CKS1B. A) CKS1B expression in pancreatic cancer compared to normal and paraneoplastic tissues in TCGA. B) CKS1B expression in pancreatic cancer compared to normal and paraneoplastic tissues in GEO. In contrast with normal tissues, cancer tissues showed higher CKS1B expression with statistical significance in TCGA (p<0.05) and GEO (p<0.0001). C) Immunohistochemistry of CKS1B in normal and tumor tissues in the the human protein atlas database. Pancreatic cancer tissues on the left and normal tissues on the right. The CKS1B showed strong positive staining results in pancreatic cancer tissues while negative in normal tissues. CKS1B: cell cycle protein-dependent kinase regulatory subunit 1B, TCGA: the cancer genome atlas, GEO: gene expression omnibus, H&E: hematoxylin and eosin, PAAD: pancreatic adenocarcinoma, IHC: immunohistochemistry

  • Figure 3
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    Figure 3

    - Clinical phenotype analysis and survival of CKS1B. A) Progression-free survival (DFS) of CKS1B expression in the GEPIA database; high CKS1B expression group (red line) was significantly lower than low CKS1B expression group (blue line); p<0.05. B) Overall survival (OS) based on K-M curve of CKS1B expression; high CKS1B expression group (red line) was lower than that of low CKS1B expression group with statistical significance (blue line); p<0.05. C-F) Relationship between CKS1B expression and clinical phenotypes such as tumor stage, lymph node metastasis, age, and alcohol consumption in the University of Alabama at Birmingham Cancer data analysis portal database. CKS1B: cell cycle protein-dependent kinase regulatory subunit 1B

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    Figure 4

    - Correlation analysis of CKS1B and miRNA. A-H) Differential expression status of hsa-miR-125a-5p, hsa-miR-369a-5p, has-miR-106a-5p, hsa-miR-150a-5P, hsa-miR-339a-5p, hsa-miR-361a-5p, hsa-miR-136a-5p, hsa-miR-20a-5P, as well as has-miR-106a-5p in the encyclopedia of RNA interactomes database versus normal tissues. CKS1B: cell cycle protein-dependent kinase regulatory subunit 1B

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    Figure 5

    - Regulatory relationship of genes co-expressed with CSK1B; A) connecting lines indicate the presence of regulation; the more connecting lines, the stronger the regulatory relationship. B&C) CKS1B enrichment analysis and co-expressed genes. Correlation analysis of PKMYT1 and CKS1B with hsa-miR-150-5P; D&E) the gene ontology as well as Kyoto encyclopedia of genes and genomes analysis of co-expressed genes in regulatory relationship with CKS1B. CKS1B: cell cycle protein-dependent kinase regulatory subunit 1B, PAAD: pancreatic adenocarcinoma

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    Figure 6

    - Signaling pathway analysis between CKS1B and PKMYT1; ATR-Chk1-Cdc25 signaling pathway involved in PKMYT1 during the cell cycle. CKS1B: cell cycle protein-dependent kinase regulatory subunit 1B, PAAD: pancreatic adenocarcinoma

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Saudi Medical Journal: 45 (2)
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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
Saudi Medical Journal Feb 2024, 45 (2) 128-138; DOI: 10.15537/smj.2024.45.2.20230132

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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
Saudi Medical Journal Feb 2024, 45 (2) 128-138; DOI: 10.15537/smj.2024.45.2.20230132
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Keywords

  • pancreatic cancer
  • regulatory subunit 1B
  • PKMYT1
  • microRNAs

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