CKS2 Predicts A Poor Prognosis and Contributes to Malignant Progression of Pancreatic Cancer
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.
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Posted 18 Jun, 2020
On 17 Jun, 2020
On 16 Jun, 2020
On 16 Jun, 2020
On 16 Jun, 2020
CKS2 Predicts A Poor Prognosis and Contributes to Malignant Progression of Pancreatic Cancer
Posted 18 Jun, 2020
On 17 Jun, 2020
On 16 Jun, 2020
On 16 Jun, 2020
On 16 Jun, 2020
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