甲基丙烯酸缩水甘油酯通过ERK/MMP14信号通路影响16HBE细胞恶性转化的研究

doi:10.3969/j.issn.1004-616x.2024.04.003

Abstract

Abstract: OBJECTIVE：To investigate whether glycidyl methacrylate (GMA) would affect malignant transformation of human bronchial epithelial (16HBE) cells through the ERK/MMP14 signaling pathway，and to investigate its molecular mechanism for malignant transformation of the 16HBE cells. METHODS：16HBE cells which were repeatedly exposed to 8 μg/mL GMA were used as the GMA treatment group，and the cells treated with the same volume of dimethyl sulfoxide (DMSO) as the solvent control group. At the 40th passage of the 16HBE cells，they were harvested，and the degree of malignant transformation was identified using the soft agar clone formation assay. The wound healing and the transwell cell migration assays were used to detect the migration ability of cells. Western blot was used to verify expression of the MMP14 protein，and levels of ERK1/2 and its phosphorylated proteins. Quantitative real-time PCR (qPCR) was used to detect mRNA expression levels of MMP14 and of the key signal molecules of the ERK pathway：ERK1 and ERK2. RESULTS：The number of colonies formed by cells in the GMA-treated group in soft agar was greater than that in the DMSO-treated group (P<0.05). Results from the wound healing and the transwell cell migration assays showed that the migration ability of the GMA-treated 16HBE cells were significantly higher than those of the DMSO-treated control cells (P<0.05). Compared with the control cells，expression levels of MMP14 mRNA and protein in 16HBE cells were increased. The expression levels of p-ERK1/2 protein and ERK1 mRNA were also increased，and the differences were statistically significant (P<0.05)，while there was no significant difference in ERK2 mRNA expression (P<0.05). CONCLUSION：The process of GMA-induced malignant transformation of 16HBE cells was associated with activation of the ERK/MMP14 signaling pathway. Our results are helpful for a better understanding of mechanism in GMA-induced malignant transformation of 16HBE cells.

Key words: glycidyl methacrylate, 16HBE cells, MMP14, ERK1/2

CLC Number:

R730.2

CUI Xufang, WANG Quankai, JIN Huiping, LI Xinwei, GU Yiting, WUHAN Baolier, KANG Tongying, XU Jianning. Glycidyl methacrylate affects malignant transformation of 16HBE cells through the ERK/MMP14 signaling pathway[J]. Carcinogenesis, Teratogenesis & Mutagenesis, 2024, 36(4): 261-267.

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Glycidyl methacrylate affects malignant transformation of 16HBE cells through the ERK/MMP14 signaling pathway

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