CTSZ Promotes HCC Metastasis
Author Information
Author(s): Wang Jian, Chen Leilei, Li Yan, Guan Xin-Yuan
Primary Institution: The University of Hong Kong
Hypothesis
The study aims to characterize the oncogenic function and mechanism of Cathepsin Z (CTSZ) in hepatocellular carcinoma (HCC).
Conclusion
CTSZ is frequently upregulated in HCC and contributes to tumor metastasis by inducing epithelial-mesenchymal transition.
Supporting Evidence
- CTSZ was upregulated in 43% of primary HCCs.
- CTSZ upregulation was significantly associated with advanced clinical stage.
- CTSZ increased colony formation in soft agar and promoted cell motility.
- CTSZ induced epithelial-mesenchymal transition by upregulating mesenchymal markers and downregulating epithelial markers.
Takeaway
This study found that a protein called Cathepsin Z helps cancer cells move and spread in the body, making the cancer worse.
Methodology
Real-time PCR, soft agar, wound-healing, transwell invasion, cell adhesion assays, and tumor xenograft mouse model were used to study CTSZ's role.
Limitations
The study was conducted using an ectopic overexpression system, which may not fully represent natural conditions.
Participant Demographics
The study included 137 pairs of human HCC and corresponding nontumorous liver tissues.
Statistical Information
P-Value
0.000
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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