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Snail as a key regulator of PRL-3 gene in colorectal cancer
Ping Zheng1, Hui-Min Meng, Wei-Zhe Gao
1Department of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Abstract:
The regulators of a key metastasis gene PRL-3 in colorectal cancer (CRC) are still largely unknown. We found three potential binding sites of Snail, a key transcriptional factor involved in the epithelial-mesenchymal transition (EMT), in the region of PRL-3 promoter (located at -642 to -383). Moreover, our results showed that one of the Snail binding sites (located at -624 to -619) was the key element to maintain promoter activity of human PRL-3 gene. The transcriptional activity of PRL-3 promoter was abolished after the Snail binding site (located at -624 to -619) was mutated. Both promoter activity and protein expression of PRL-3 in CRC cell lines could be regulated by Snail. In clinical samples of CRC and metastatic lymph node of CRC, expression of PRL-3 protein was correlated with expression of Snail protein. Functional studies using gene over-expression and knockdown methods indicated that Snail promoted proliferation, cell adhesion and migration of human CRC cells. In SW480 cells with PRL-3 stable knockdown, cell proliferation increased after Snail was up-regulated. Our data first reveal transcriptional factor Snail as a key regulator of PRL-3 in CRC. The link between Snail and PRL-3 suggests a new potential mechanism of Snail contributing to progression and metastasis of CRC.
Insights
Transcriptional factor Snail regulates the metastasis gene PRL-3 in colorectal cancer (CRC). Snail controls PRL-3 expression, impacting CRC cell proliferation, adhesion, and migration, suggesting a new mechanism for cancer progression.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Genetics
Background:
- The regulators of the metastasis gene PRL-3 in colorectal cancer (CRC) are largely unknown.
- PRL-3 is implicated in cancer progression and metastasis.
- Snail is a key transcriptional factor involved in epithelial-mesenchymal transition (EMT).
Purpose of the Study:
- To identify regulators of the PRL-3 gene in colorectal cancer.
- To investigate the role of the transcriptional factor Snail in regulating PRL-3 expression and function in CRC.
Main Methods:
- Promoter analysis to identify Snail binding sites in the PRL-3 gene promoter region.
- Site-directed mutagenesis to assess the functional significance of Snail binding sites.
- Gene over-expression and knockdown studies in CRC cell lines.
- Analysis of PRL-3 and Snail protein expression in clinical CRC samples.
Main Results:
- Three potential Snail binding sites were identified in the PRL-3 promoter region (-642 to -383).
- A specific Snail binding site (-624 to -619) was crucial for maintaining human PRL-3 promoter activity; mutation abolished activity.
- Snail regulates both PRL-3 promoter activity and protein expression in CRC cell lines.
- PRL-3 protein expression correlated with Snail protein expression in clinical CRC and metastatic lymph node samples.
- Snail promoted CRC cell proliferation, adhesion, and migration.
- In cells with reduced PRL-3, Snail up-regulation increased cell proliferation.
Conclusions:
- Transcriptional factor Snail is identified as a key regulator of PRL-3 in colorectal cancer.
- The Snail-PRL-3 interaction provides a novel mechanistic insight into Snail's contribution to CRC progression and metastasis.
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