Open Access

MiR-19a-3p/PTEN axis regulates the anticancer effect of circHIAT1 in breast cancer in vitro

by CHAO NIU^1,#, RUOFEI SUN^1,#, XIAOGANG LI², BO LI², XIAODONG HE^1,*

1 Department of General Surgery, Lanzhou University Second Hospital, Lanzhou, 730000, China
2 Department of General Surgery, Affiliated Hospital of Yunnan University, Kunming, 650051, China

* Corresponding Author: XIAODONG HE. Email:
# These authors contributed equally

(This article belongs to the Special Issue: Non-Coding RNAs in the Regulation of Human Cancers)

BIOCELL 2023, 47(10), 2301-2312. https://doi.org/10.32604/biocell.2023.029935

Received 15 March 2023; Accepted 26 June 2023; Issue published 08 November 2023

Abstract

Objective: Breast cancer is a major cancer threatening the health of women globally. To elucidate the effect of the circHIAT1/miR-19a-3p/phosphatase and tensin homolog (PTEN) axis on regulating the malignant phenotype of breast cancer cells. Methods: The mRNA expression pattern of circHIAT1, miR-19a-3p, and PTEN was checked by real-time quantitative polymerase chain reaction. Then, the knockdown assay was carried out to explore the effect of circHIAT1 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-3p was elevated in breast cancer tissues and cells. MiR-19a-3p was proved to be the target gene of circHIAT1 via a dual luciferase experiment, which could also modulate the PTEN mRNA level. Overexpression of circHIAT1 was able to undermine 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 depended on the modulation of PTEN expression. Conclusion: CircHIAT1 controls the PTEN expression level in cells of breast cancer by negatively regulating miR-19a-3p. This mechanism controls the growth, invasion, and migration of breast cancer.

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