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Knockdown of SPOCK1 Inhibits the Proliferation and Invasion in Colorectal Cancer Cells by Suppressing the PI3K/Akt
Ping Zhao1, Hai-Tao Guan, Zhi-Jun Dai
1Department of Gastroenterology, the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi Province, P.R. China.
Abstract:
Sparc/osteonectin, cwcv, and kazal-like domains proteoglycan (testican) 1 (SPOCK1), known as testican-1, were found to be involved in the development and progression of tumors. However, in colorectal cancer (CRC), the expression pattern of SPOCK1 and its functional role remain poorly investigated. In the present study, we explored the role of SPOCK1 in CRC. Our results demonstrated that SPOCK1 is overexpressed in CRC cell lines. SPOCK1 silencing significantly inhibited the proliferation in vitro and the tumor growth in vivo. Furthermore, SPOCK1 silencing significantly attenuated the migration/invasion by reversing the EMT process in CRC cells. Finally, knockdown of SPOCK1 obviously decreased the protein expression levels of p-PI3K and p-Akt in HCT116 cells. In total, our study demonstrated for the first time that knockdown of SPOCK1 inhibits the proliferation and invasion in CRC cells, possibly through the PI3K/Akt signaling pathway. Therefore, SPOCK1 may be a potential therapeutic target for the treatment of CRC.
Insights
Sparc/osteonectin, cwcv, and kazal-like domains proteoglycan 1 (SPOCK1) is overexpressed in colorectal cancer (CRC). Silencing SPOCK1 inhibits CRC cell proliferation and invasion, suggesting it as a potential therapeutic target.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Sparc/osteonectin, cwcv, and kazal-like domains proteoglycan 1 (SPOCK1), or testican-1, is implicated in tumor development.
- The role and expression of SPOCK1 in colorectal cancer (CRC) are not well understood.
Purpose of the Study:
- To investigate the expression pattern and functional role of SPOCK1 in colorectal cancer.
- To explore SPOCK1 as a potential therapeutic target for CRC treatment.
Main Methods:
- SPOCK1 expression analysis in CRC cell lines.
- In vitro and in vivo studies involving SPOCK1 silencing.
- Assessment of cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT).
- Western blot analysis to evaluate PI3K/Akt signaling pathway activation.
Main Results:
- SPOCK1 is significantly overexpressed in CRC cell lines.
- SPOCK1 knockdown suppressed CRC cell proliferation in vitro and tumor growth in vivo.
- Silencing SPOCK1 attenuated migration and invasion by reversing EMT.
- Knockdown of SPOCK1 decreased the phosphorylation of PI3K and Akt.
Conclusions:
- SPOCK1 knockdown inhibits proliferation and invasion in colorectal cancer cells.
- The PI3K/Akt signaling pathway is implicated in SPOCK1's effects on CRC.
- SPOCK1 represents a potential therapeutic target for colorectal cancer.
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