Objective: Breast cancer is a major cancer threatening the health of women globally. To elucidate the effect ofthe circHIAT1/miR-19a-3p/phosphatase and tensin homolog (PTEN) axis on regulating the malignant phenotype ...Objective: Breast cancer is a major cancer threatening the health of women globally. To elucidate the effect ofthe circHIAT1/miR-19a-3p/phosphatase and tensin homolog (PTEN) axis on regulating the malignant phenotype ofbreast cancer cells. Methods: The mRNA expression pattern of circHIAT1, miR-19a-3p, and PTEN was checked byreal-time quantitative polymerase chain reaction. Then, the knockdown assay was carried out to explore the effect ofcircHIAT1 and miR-19a-3p on breast cancer. The relative cell experiments, including MTT assay, scratch assay,transwell invasion assay, and flow cytometry analysis, were conducted to verify the influence of circHIAT1 and miR-19a-3p on breast cancer cells. Results: The levels of PTEN and circHIAT1 were reduced, while that of miR-19a-3pwas elevated in breast cancer tissues and cells. MiR-19a-3p was proved to be the target gene of circHIAT1 via a dualluciferase experiment, which could also modulate the PTEN mRNA level. Overexpression of circHIAT1 was able toundermine the growth, migratory ability, and invasiveness in breast cancer cells, which could be antagonized by miR-19a-3p mimic. The inhibition of miR-19a-3p in vitro also impaired the malignancy of breast cancer, which dependedon the modulation of PTEN expression. Conclusion: CircHIAT1 controls the PTEN expression level in cells of breastcancer by negatively regulating miR-19a-3p. This mechanism controls the growth, invasion, and migration of breastcancer.展开更多
基金All experimental procedures were conducted in accordance with Animal Ethics Procedures and Guidelines of the Animal Center,Yunnan University Animal Ethics Committee(Ethics Review Number:YNU20220296).
文摘Objective: Breast cancer is a major cancer threatening the health of women globally. To elucidate the effect ofthe circHIAT1/miR-19a-3p/phosphatase and tensin homolog (PTEN) axis on regulating the malignant phenotype ofbreast cancer cells. Methods: The mRNA expression pattern of circHIAT1, miR-19a-3p, and PTEN was checked byreal-time quantitative polymerase chain reaction. Then, the knockdown assay was carried out to explore the effect ofcircHIAT1 and miR-19a-3p on breast cancer. The relative cell experiments, including MTT assay, scratch assay,transwell invasion assay, and flow cytometry analysis, were conducted to verify the influence of circHIAT1 and miR-19a-3p on breast cancer cells. Results: The levels of PTEN and circHIAT1 were reduced, while that of miR-19a-3pwas elevated in breast cancer tissues and cells. MiR-19a-3p was proved to be the target gene of circHIAT1 via a dualluciferase experiment, which could also modulate the PTEN mRNA level. Overexpression of circHIAT1 was able toundermine the growth, migratory ability, and invasiveness in breast cancer cells, which could be antagonized by miR-19a-3p mimic. The inhibition of miR-19a-3p in vitro also impaired the malignancy of breast cancer, which dependedon the modulation of PTEN expression. Conclusion: CircHIAT1 controls the PTEN expression level in cells of breastcancer by negatively regulating miR-19a-3p. This mechanism controls the growth, invasion, and migration of breastcancer.
