Citation: | CHEN Bai-sheng, LI Ping, ZHOU Ying, et al. The role of promyelocytic leukemia protein in the carcinogenesis of colorectal adenoma[J]. Chin J Clin Med, 2022, 29(1): 23-29. DOI: 10.12025/j.issn.1008-6358.2022.20211765 |
To analyze expression of promyelocytic leukemia protein (PML) in colorectal adenoma, colorectal cancer tissues, and colorectal cancer cells, and to explore the role of PML in the occurrence and development of colorectal cancer.
The expression level of PML in colorectal cancer, colorectal adenoma, and normal colorectal mucosa were detected by immunohistochemistry and Western blotting. The expression of PML in 10 different colorectal cancer cell lines were detected, and suitable cell lines were screened for further cell migration, and invasion tests. Furthermore, PML silenced and overexpressed colorectal cancer cell models were established, and cell migration, invasion, proliferation, and apoptosis experiments were performed. The effects of PML on vascular endothelial growth factor (VEGF) and epidermal growth factor receptor (EGFR) expressions were analyzed.
Compared with normal tissue, the expression of PML decreased in adenoma tissue and further decreased in colorectal cancer tissue (P < 0.05). Among the 10 different colorectal cancer cell lines, the cells with lower PML expression were more invasive. After silencing PML, the migration, invasion, and proliferation rates of colorectal cancer cells increased, and apoptosis decreased (P < 0.05); while the migration, invasion, and proliferation rates of colorectal cancer cells decreased with high expression of PML, and apoptosis increased (P < 0.05). After silencing PML, the expressions of EGFR and VEGF in colorectal cancer cells were significantly increased (P < 0.05); while the expressions of EGFR and VEGF in colorectal cancer cells decreased significantly with high PML expression (P < 0.05).
PML is lowly expressed in colorectal adenoma tissue, and its expression is further reduced in colorectal cancer tissue. PML can inhibit the migration, invasion, and proliferation of colorectal cancer cells, and promote their apoptosis, through the negative regulation of VEGF and EGFR.
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