- Adipose Tissue-Derived Stem Cells
- Human Neurons
- Mouse Probe
- Whole Chromosome Painting Probes
- Hepatic Cells
- Renal Cells
- In Vitro ADME Kits
- Tissue Microarray
- Tissue Blocks
- Tissue Sections
- FFPE Cell Pellet
- Probe
- Centromere Probes
- Telomere Probes
- Satellite Enumeration Probes
- Subtelomere Specific Probes
- Bacterial Probes
- ISH/FISH Probes
- Exosome Isolation Kit
- Human Adult Stem Cells
- Mouse Stem Cells
- iPSCs
- Mouse Embryonic Stem Cells
- iPSC Differentiation Kits
- Mesenchymal Stem Cells
- Immortalized Human Cells
- Immortalized Murine Cells
- Cell Immortalization Kit
- Adipose Cells
- Cardiac Cells
- Dermal Cells
- Epidermal Cells
- Peripheral Blood Mononuclear Cells
- Umbilical Cord Cells
- Monkey Primary Cells
- Mouse Primary Cells
- Breast Tumor Cells
- Colorectal Tumor Cells
- Esophageal Tumor Cells
- Lung Tumor Cells
- Leukemia/Lymphoma/Myeloma Cells
- Ovarian Tumor Cells
- Pancreatic Tumor Cells
- Mouse Tumor Cells
Our Promise to You
Guaranteed product quality, expert customer support
Loss of cyclin‐dependent kinase‐like 2 predicts poor prognosis in gastric cancer, and its overexpression suppresses cells growth and invasion
PMID:29790675
Abstract
BACKGROUND: Cyclin‐dependent kinase‐like 2 (CDKL2), a new member of the cyclin‐dependent kinase family, may be involved in gastric cancer (GC) progression.
METHODS: Thus, we conducted this study to explore the clinical effect of CDKL2 in GC. Immunohistochemistry was used to measure CDKL2 levels in gastric tissues. The association of a high CDKL2 level with clinical and pathological characteristics, and the correlation between the CDKL2 level and disease‐free and overall survival were analyzed. Transfection was employed to overexpress CDKL2 in GC cells and to investigate the effect of CDKL2 overexpression on cell proliferation and invasion.
RESULTS: Loss of CDKL2 was positively correlated with several clinical and pathological characteristics, and patients with a low CDKL2 level had significantly poorer disease‐free and overall survival than those with a high level (P = .005 and .001, respectively). Univariate analysis using the Cox proportional hazards model indicated that a low CDKL2 level was a prognosticator for inferior disease‐free survival (P = .007). Based on immmunoblotting data, AGS and HGC‐27 GC cells were chosen for CDKL2 overexpression. Cellular studies revealed that CDKL2 overexpression impaired cell proliferation and invasion.
CONCLUSION: Loss of CDKL2 may serve as a biomarker for predicting GC patient outcomes and a potential therapeutic target for GC treatment.