4.1 Article

LncRNA ZFAS1/miR-589 regulates the PTEN/PI3K/AKT signal pathway in the proliferation, invasion and migration of breast cancer cells

期刊

CYTOTECHNOLOGY
卷 72, 期 3, 页码 415-425

出版社

SPRINGER
DOI: 10.1007/s10616-020-00388-6

关键词

LncRNA ZFAS1; miR-589; Proliferation; Invasion; Migration; Breast cancer cells

资金

  1. Science and Technology Development Fund Project of Bengbu Medical College [BYKF1866]
  2. National Natural Science Foundation Item [81572992]

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Breast cancer (BC) is a common clinical disease and the second leading cause of cancer death in women. Long noncoding RNA (lncRNA) and microRNA (miRNA) are reported to be involved in the development of BC. The present study aimed to investigate whether LncRNA ZFAS1 could regulate the proliferation, invasion and migration of breast cancer cells by targeting miR-589 through PTEN/PI3K/AKT signal pathway. The expression of ZFAS1 and miR-589 in BC cells and transfection effects were determined by RT-qPCR analysis. The abilities of proliferation, colony formation, invasion and migration of breast cancer cells were analyzed by CCK-8 assay, colony formation assay, transwell assay and wound healing assay respectively. The expression of MMP2, MMP9, Bcl2, Bax, cleaved caspase3, PTEN, p-PI3K, p-AKT, PI3K and AKT was detected by Western blot. The flow cytometry analysis was used to detect cell apoptosis. As a result, ZFAS1 expression was increased and miR-589 expression was decreased in BC cells. And, miR-589 was demonstrated to be a target of ZFAS1. ZFAS1 overexpression could inhibit the proliferation, colony formation, invasion and migration of BC cells while miR-589 overexpression could reverse the changes. In addition, ZFAS1 overexpression suppressed the expression of PI3K/AKT signal pathway by activating the PTEN expression while miR-589 overexpression could reverse the changes. Moreover, PTEN is one of the gene targets of miR-589. In conclusion, this study indicated that ZFAS1 inhibited the proliferation, invasion and migration of breast cancer cells by targeting miR-589 through regulating the PTEN/PI3K/AKT signal pathway.

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