Long non-coding RNA (lncRNA) MALAT1 has been confirmed to function as an oncogene in various solid tumors. MALAT1 level has been shown to be upregulated in relapsed acute lymphoblastic leukemia (ALL) patients, but the mechanism is unclear. This study aims to investigate the functional roles and underlying mechanisms of MALAT1 in ALL. MALAT1 and miR-205 expression were assessed by real-time quantitative polymerase chain reaction (RT-qPCR). MTT assay and flow cytometry were performed to evaluate cell proliferation and apoptosis, respectively. Protein level of protein tyrosine kinase-7 (PTK7) was detected by Western blot assay. Dual luciferase reporter assay was conducted to confirm the binding of MALAT1 and miR-205, as well as miR-205 and PTK7. The levels of MALAT1 and PTK7 were upregulated in ALL samples. In contrast, miR-205 level was downregulated in ALL in ALL samples. Moreover, MALAT1 silencing or miR-205 overexpression restrained proliferation and promoted apoptosis of ALL cells. Mechanistically, MALAT1 sponged miR-205 to regulate PTK7 expression. In summary, MALAT1 affected ALL cell proliferation and apoptosis via regulating miR-205-PTK7 axis. Our results suggest that MALAT1-miR-205-PTK7 axis participates in the proliferation and apoptosis of ALL, which may provide a potential treatment target for ALL.
Keywords: MALAT1; PTK7; acute lymphoblastic leukemia; lncRNA; miR-205.
© 2020 Japanese Society of Pathology and John Wiley & Sons Australia, Ltd.