LINC00324 suppresses abnormal proliferation and promotes apoptosis of leukemia cells through the miR-10b-5p/PTEN pathway.

Abstract

Long non-coding RNAs (lncRNAs) are known to participate in leukemia development, but the molecular mechanisms of many remain unclear. The expression of LINC00324 was examined in peripheral blood samples from leukemia patients and in leukemia cell lines by RT-qPCR. Functional studies were performed to evaluate how LINC00324 overexpression or knockdown affected cell proliferation and apoptosis. Flow cytometry was used to detect apoptosis. Western blotting was applied to measure Ki-67, BAX, Bcl-2, and PTEN protein levels. Dual-luciferase reporter assays were used to confirm the interaction among LINC00324, miR-10b-5p, and PTEN. LINC00324 expression was markedly reduced in leukemia samples and cell lines. Upregulation of LINC00324 inhibited the proliferation of Jurkat and HL-60 cells and increased apoptosis, while its silencing produced the opposite trend. Western blotting showed that LINC00324 overexpression decreased Ki-67 and Bcl-2 but increased BAX expression. Rescue experiments demonstrated that miR-10b-5p mimics reversed, whereas inhibitors restored, the effects of LINC00324. Bioinformatics prediction and luciferase validation identified PTEN as a direct target of miR-10b-5p, and LINC00324 enhanced PTEN expression by sponging miR-10b-5p. LINC00324 regulates the proliferation and apoptosis of leukemia cells through the miR-10b-5p/PTEN axis. These findings add to the understanding of lncRNA-mediated regulatory mechanisms in leukemia.