Cyclin b1 suppresses colorectal cancer invasion and metastasis by regulating e-cadherin.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 25962181.
- Also identified by DOI 10.1371/journal.pone.0126875 and PMC identifier 4427130.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
Abstract
Cyclin B1, a mitotic cyclin, has been implicated in malignances. However, its contribution to colorectal cancer invasion and metastasis are still not well understood. Here, we demonstrated that the invasion and metastasis of colorectal cancer is regulated by Cyclin B1. Overexpression of Cyclin B1 was observed in colorectal cancer tissues, but this elevated expression was negatively associated with lymph node metastasis, distant metastasis stage, and TNM stage. The Kaplan-Meier survival analysis proved that low Cyclin B1 expression was associated with poor overall survival of patients with colorectal cancer. Inhibition of Cyclin B1 in colorectal cancer cells enhanced the cell migration and invasion of three different colorectal cancer cell lines. In studying the possible mechanism by which Cyclin B1 suppresses colorectal cancer invasion and metastasis, we observed that suppression of Cyclin B1 decreased the expression of E-cadherin protein level. Our findings suggest that Cyclin B1 could suppress the invasion and metastasis of colorectal cancer cells through regulating E-cadherin expression, which enables the development of potential intervention strategies for colorectal cancer.
Medical subject headings
- Cadherins
- Colorectal Neoplasms
- Cyclin B1