This preprint is under consideration at Journal of Experimental & Clinical Cancer Research. A preprint is a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
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CKS2 Predicts A Poor Prognosis and Contributes to Malignant Progression of Pancreatic Cancer
Junli Wu
First Affiliated Hospital of Nanjing Medical University
Corresponding Author
ORCiD: https://orcid.org/0000-0002-6946-0510
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background: Cyclin-dependent kinase subunit 2 (CKS2) has been reported to promote various malignancies. This study aims to investigate the prognostic significance and functional role of CKS2 in pancreatic cancer.
Methods: The analysis of abnormal expression genes and prognosis value on pancreatic cancer by Gene Expression Profiling Interactive Analysis (GEPIA) database and immunohistochemical staining of 64 samples of tumors. CCK-8 assay, EdU staining, colony formation, flow cytometry, wound healing assay, transwell assay, and a xenograft tumor model were used to analyze the biological function of CKS2 in pancreatic cancer. Western blotting was performed to explore the mechanisms underlying the effect of CKS2 on cell cycle progression and apoptosis.
Results: A significantly higher expression of CKS2 was found in pancreatic cancer compared with adjacent normal tissues and high CKS2 expression indicated poor prognosis in patients with pancreatic cancer. Moreover, functional assays revealed that CKS2 knockdown suppressed cell proliferation, migration and invasion ability, induced cell cycle G2/M phase arrest and apoptosis in vitro and reduced tumor growth in vivo. In addition, CKS2 knockdown increased the expression of Bax, caspase-3, P53, P21 and GADD45α, but decreased the expression of Bcl-2, Cyclin B1, CDK1, Cyclin A, and Cdc25C. CKS2 overexpression obtained the opposite results to CKS2 knockdown.
Conclusions: Our findings suggested that CKS2 may act as a promising prognostic indicator and therapeutic target for the treatment of pancreatic cancer.
Keywords
CKS2, pancreatic cancer, prognosis, G2/M phase, apoptosis
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This preprint is under consideration at Journal of Experimental & Clinical Cancer Research. A preprint is a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Learn more about In Review
Research
CKS2 Predicts A Poor Prognosis and Contributes to Malignant Progression of Pancreatic Cancer
Junli Wu
First Affiliated Hospital of Nanjing Medical University
Corresponding Author
ORCiD: https://orcid.org/0000-0002-6946-0510
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
Peer Review Timeline
CURRENT STATUS: Under Review
Version 1
Posted 18 Jun, 2020
No community comments so far
Editor assigned
On 17 Jun, 2020
First submitted
On 16 Jun, 2020
Submission checks complete
On 16 Jun, 2020
Editor invited
On 16 Jun, 2020
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background: Cyclin-dependent kinase subunit 2 (CKS2) has been reported to promote various malignancies. This study aims to investigate the prognostic significance and functional role of CKS2 in pancreatic cancer.
Methods: The analysis of abnormal expression genes and prognosis value on pancreatic cancer by Gene Expression Profiling Interactive Analysis (GEPIA) database and immunohistochemical staining of 64 samples of tumors. CCK-8 assay, EdU staining, colony formation, flow cytometry, wound healing assay, transwell assay, and a xenograft tumor model were used to analyze the biological function of CKS2 in pancreatic cancer. Western blotting was performed to explore the mechanisms underlying the effect of CKS2 on cell cycle progression and apoptosis.
Results: A significantly higher expression of CKS2 was found in pancreatic cancer compared with adjacent normal tissues and high CKS2 expression indicated poor prognosis in patients with pancreatic cancer. Moreover, functional assays revealed that CKS2 knockdown suppressed cell proliferation, migration and invasion ability, induced cell cycle G2/M phase arrest and apoptosis in vitro and reduced tumor growth in vivo. In addition, CKS2 knockdown increased the expression of Bax, caspase-3, P53, P21 and GADD45α, but decreased the expression of Bcl-2, Cyclin B1, CDK1, Cyclin A, and Cdc25C. CKS2 overexpression obtained the opposite results to CKS2 knockdown.
Conclusions: Our findings suggested that CKS2 may act as a promising prognostic indicator and therapeutic target for the treatment of pancreatic cancer.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6