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Archive > Volume 31 Issue 7 > 2024,31(7):687-693. DOI:10.3872/j.issn.1007-385X.2024.07.007 Prev Next
Basic Research
Effects of pristimerin on the proliferation, apoptosis and vasculogenic mimicry of cervical cancer HeLa cells by regulating the Shh/Gli1 signaling pathway
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Abstract:
Objective: To investigate the effects of pristimerin (Pris) on the proliferation, apoptosis and vasculogenic mimicry (VM) of cervical cancer HeLa cells by regulating the Shh/Gli1 signaling pathway. Methods: MTT method was used to detect the inhibitory effects of Pris in different concentrations on the proliferation of cervical-cancer HeLa cells to select appropriate intervention concentration. Cervical cancer HeLa cells were grouped into the control group, the cyclopamine group, the Pris group, the Pris+pc-NC group and the Pris+pc-Shh group. MTT and EdU were applied to detect the proliferation abilities of cells in each group. Transwell chamber method and flow cytometry were used to detect cell migration and invasion abilities and cell apoptosis rate. In vitro angiogenesis experiments were used to observe the formation of VM. qPCR was used to detect Shh and Gli1 mRNA expression levels in each group. Western blotting was used to detect the expression levels of vascular endothelial growth factor A (VEGF-A), vascular endothelial cadherin (VE-cadherin), Ki-67, caspase-3, and proteins related to the Shh/Gli1 signaling pathway. Results: 0.25-2.5 mol/L Pris significantly inhibited the proliferation of HeLa cells, and 1.5 mol/L was selected for subsequent experiments. The cells in the control group formed a good lumen structure. Compared with the control group, the lumen structures of HeLa cells in the cyclopamine group, the Pris group and the Pris+pc-NC group were significantly damaged. Cell proliferation activity, proliferation rate, numbers of migration and invasion, expression levels of Shh and Gli1 mRNA, and expression levels of VEGF-A, VE-cadherin, Ki-67, Shh and Gli1 proteins were significantly decreased (all P<0.05). The apoptosis rate and the expression level of caspase-3 were significantly increased (all P<0.05). There was no significant difference in HeLa cell detection indicators between the cyclopamine group and the Pris group (all P>0.05). Compared with the Pris+pc-NC group, the formation of cell lumen structure in the Pris+pc-Shh group was significantly improved. The cell proliferation activity and proliferation rate, the numbers of migration and invasion cells, the expressions of Shh and Gli1 mRNA, and the expressions of VEGF-A, VE-cadherin, Ki-67, Shh and Gli1 proteins were significantly increased (all P<0.05). The apoptosis rate and the expression level of caspase-3 were significantly decreased (all P<0.05). Conclusion: Pris can inhibit the proliferation, migration, invasion and VM formation of cervical cancer HeLa cells, and promote cell apoptosis, which may be related to blocking the Shh/Gli1 signaling pathway.
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