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Updated: Feb 15, 2026

Induction and Analysis of Epithelial to Mesenchymal Transition
Published on: August 27, 2013
NEK2 promotes hepatocellular carcinoma migration and invasion through modulation of the epithelial-mesenchymal
Yi Zhang1, Wei Wang2, Yifei Wang1
1Department of Hepatic Surgery, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, Guangdong 510080, P.R. China.
Abstract:
Never in mitosis gene-A (NIMA)-related expressed kinase 2 (NEK2) has been recently reported to play a role in tumor progression, drug resistance and tumorigenesis. However, little is known about the effects of NEK2 in hepatocellular carcinoma (HCC) metastasis and the underlying mechanism. NEK2 expression levels were examined by immunochemistry, qRT‑PCR and western blot analyses in HCC cell lines and HCC tissues. A Transwell assay was used to determine the migration and invasion capacity of NEK2-silenced or NEK2-overexpressing HCC cells. Cell proliferation was investigated by MTT [(3-(4,5)-dimethylthiazol(-z-y1)-3,5-di-phenytetrazolium bromide] assay. The expression levels of epithelial-mesenchymal transition (EMT) markers in NEK2-silenced or NEK2-overexpressing HCC cells were examined by western blot analyses and qRT‑PCR. The correlations between NEK2 expression and clinicopathological characteristics were further analyzed. Gene microarray was further used to analyze the effect of NEK2 expression on downstream cell signals. Our study showed that NEK2 was overexpressed in human HCC (37.84%; 98/259). NEK2 overexpression was significantly associated with liver non‑capsulation and predicted poor survival outcomes in HCC patients after hepatectomy. In addition, NEK2 significantly enhanced HCC cell invasive ability. Mechanistically, we found that the epithelial-mesenchymal transition (EMT) plays a pivotal role in the NEK2-mediated promotion of HCC cell invasion. Furthermore, we provided evidence that signaling through the Wnt, NF-κB, focal adhesion, VEGF, Hippo and p53 pathways may be downstream of NEK2. Our findings highlight the importance of NEK2 in HCC metastasis and suggest that NEK2 is a reliable prognostic marker for HCC patients after hepatectomy.
Insights
Never in mitosis gene-A (NIMA)-related expressed kinase 2 (NEK2) promotes hepatocellular carcinoma (HCC) metastasis by enhancing cell invasion. NEK2 overexpression is linked to poor survival and may serve as a prognostic marker in HCC patients.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Hepatocellular carcinoma (HCC) is a major global health concern with limited treatment options.
- The role of Never in mitosis gene-A (NIMA)-related expressed kinase 2 (NEK2) in HCC metastasis remains largely unexplored.
- Understanding NEK2's function is crucial for developing novel therapeutic strategies for HCC.
Purpose of the Study:
- To investigate the expression and function of NEK2 in hepatocellular carcinoma (HCC) metastasis.
- To elucidate the underlying molecular mechanisms by which NEK2 influences HCC cell invasion.
- To evaluate NEK2 as a potential prognostic biomarker for HCC patients.
Main Methods:
- NEK2 expression was assessed using immunohistochemistry, qRT-PCR, and Western blot in HCC cell lines and tissues.
- Transwell and MTT assays were employed to evaluate cell migration, invasion, and proliferation.
- Epithelial-mesenchymal transition (EMT) markers, downstream signaling pathways (Wnt, NF-κB, focal adhesion, VEGF, Hippo, p53), and clinicopathological correlations were analyzed.
Main Results:
- NEK2 was overexpressed in 37.84% of human HCC cases and associated with non-capsulation.
- NEK2 overexpression significantly enhanced HCC cell invasion and migration.
- NEK2 promoted HCC cell invasion through the epithelial-mesenchymal transition (EMT) pathway.
Conclusions:
- NEK2 is significantly overexpressed in HCC and correlates with poor patient survival.
- NEK2 plays a critical role in promoting HCC metastasis via EMT.
- NEK2 represents a promising prognostic marker for hepatocellular carcinoma.
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