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CKS2 Promotes the Growth in Non-Small-Cell Lung Cancer by Downregulating Cyclin-Dependent Kinase Inhibitor
Zongren Wan1, Lixin Wang1, Dan Yang1
1Department of Pulmonary and Critical Care Medicine, Huai'an First People's Hospital, Huai'an, China.
Introduction/Objective:
This study aimed to explore the expression of cyclin-dependent kinase subunit 2 (CKS2) in tissues and cells in non-small-cell lung cancer (NSCLC) and the function mechanism of CKS2 in NSCLC cell growth and tumorigensis.
Methods:
After transfecting NCI-H2170 cells with short-hair RNA (shRNA), an shCKS2 gene-silencing model was established. The cells were divided into a shRNA group and shNC group. For overexpression cell lines, we used the same method to establish the NCI-H2170-CKS2 cell lines. Cell Count Kit-8 assay and colony formation assay were used to determine cell viability and cell growth, respectively. Propidium iodide staining was used to determine cell cycle progression. The mRNA expression of CKS2 and protein expression of CKS2, p21, p53, and PTEN were determined by RT-qPCR and Western blotting, respectively. The expression of CKS2, p53, and Ki67 in tissues was determined by immunohistochemical stain. The in vivo tumorigenesis assays were used to determine the ability of CKS2 in tumor growth.
Results:
The results of RT-qPCR and Western blotting assay revealed that CKS2 upregulated expression in NSCLC tissues and cells. The results of the CCK-8 assay revealed that the shRNA group exhibited significantly lower cell viability and foci formation than the empty plasmid group, while CKS2 overexpression induces cell growth and cell cycle progression. The result of nude mice suggested that CKS2 knockdown expression suppressed tumorigenesis in the in vivo animal model.
Conclusions:
Our study suggests that CKS2 could be a biomarker in the progression and prognosis of NSCLC.
Insights
Cyclin-dependent kinase subunit 2 (CKS2) is upregulated in non-small-cell lung cancer (NSCLC). Silencing CKS2 inhibits NSCLC cell growth and tumor formation, suggesting CKS2 is a potential biomarker for NSCLC progression.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Non-small-cell lung cancer (NSCLC) is a leading cause of cancer-related mortality worldwide.
- Understanding the molecular mechanisms driving NSCLC progression is crucial for developing effective therapies.
Purpose of the Study:
- To investigate the expression levels of cyclin-dependent kinase subunit 2 (CKS2) in NSCLC tissues and cells.
- To elucidate the functional role of CKS2 in NSCLC cell proliferation, cell cycle progression, and tumorigenesis.
Main Methods:
- Established gene-silencing and overexpression models of CKS2 in NCI-H2170 NSCLC cells using shRNA and plasmid transfection.
- Assessed cell viability and growth using Cell Count Kit-8 and colony formation assays.
- Analyzed cell cycle progression via propidium iodide staining.
- Quantified gene and protein expression using RT-qPCR and Western blotting.
- Evaluated in vivo tumor growth in a nude mouse model.
Main Results:
- CKS2 expression was significantly upregulated in NSCLC tissues and cells compared to controls.
- CKS2 knockdown suppressed NSCLC cell viability, proliferation, and colony formation.
- CKS2 overexpression promoted cell growth and accelerated cell cycle progression.
- In vivo studies demonstrated that CKS2 knockdown inhibited tumor formation in nude mice.
Conclusions:
- CKS2 plays a critical role in promoting NSCLC cell growth and tumorigenesis.
- CKS2 expression levels correlate with NSCLC progression.
- CKS2 represents a potential biomarker for predicting NSCLC prognosis and progression.
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