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Archive > Volume 29 Issue 8 > 2022,29(8):741-749. DOI:10.3872/j.issn.1007-385X.2022.08.006 Prev Next
Clinical Research
Overexpression of lncRNA MIR17HG promotes the malignant biological behaviors of cervical cancer HeLa cells and the growth of transplanted tumors in nude mice
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Abstract:
Objective: To investigate the expression level and clinical significance of lncRNA MIR17HG in cervical cancer tissues and cells, and to analyze its effect on the malignant biological behaviors of cervical cancer HeLa cells and the growth of transplanted tumors in nude mice and its possible mechanism. Methods: The TCGA database was used to analyze the expression levels of MIR17HG and TRIM25 in cervical cancer tissues, and to analyze the correlation between their expression levels and the clinicopathological characteristics of patients. The tumor tissues and paracancerous tissues of 30 cervical cancer patients admitted to Qilu Hospital of Shandong University from August 2019 to December 2020 were collected. Human normal cervical epithelial End1/E6E7 cells and human breast cancer cells HeLa, C33A, CasKi and SiHa were cultured in vitro. qPCR was used to detect the expression level of MIR17HG in cervical cancer tissues and cells. The MIR17HG overexpression plasmid or knockdown plasmid was transfected into cervical cancer HeLa cells by liposomes respectively, and then the impact of MIR17HG on the proliferation, colony formation,migration, and invasion abilities on HeLa cells were detected by CCK-8 assay, colony formation assay and Transwell assay,respectively. The targeted regulation of MIR17HG on TRIM25 was predicted by ENCORI and verified by qPCR and WB methods.Targetscan and fluorescent reporter systems were used to verify the targeting relationship between miR-377 and TRIM25. WB method was used to detect the effect of MIR17HG on the expression of AKT signaling pathway-related proteins in HeLa cells. A nude mouse xenograft model of MIR17HG overexpressing HeLa cells was constructed, and the growth of the transplanted tumor was observed.Results: Both MIR17HG and TRIM25 mRNA were highly expressed in cervical cancer tissues (both P<0.05), and the expression level of MIR17HG in cervical cancer cells was higher than that in human normal cervical epithelial cells (P<0.01 or P<0.001). The high expression of MIR17HG and TRIM25 was associated with the malignancy of cervical cancer (P<0.05). Compared with the control group, the proliferation, colony formation, migration, and invasion abilities of HeLa cells in the MIR17HG overexpression group were significantly increased, while the opposite was true in the MIR17HG knockdown group (P<0.05 or P<0.01). MIR17HG may upregulate the expression of TRIM25 by inhibiting miR-377. The expression levels of AKT signaling pathway-related proteins in HeLa cells in the MIR17HG overexpression group were increased. The growth level of xenograft tumors in the MIR17HG overexpression group was higher than that in the control group (P<0.01). Conclusion: MIR17HG is highly expressed in cervical cancer tissues and cells. Overexpression of MIR17HG can promote the malignant biological behaviors of HeLa cells and accelerate the growth of transplanted tumors in nude mice. MIR17HG may exert its cancer-promoting effect by inhibiting miR-377 and upregulating TRIM25 to activate the AKT pathway.
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