Supplementary Material for: LINC01002 targets miR-650/FLNA pathway to suppress prostate cancer progression

Introduction: In view of the vital implication of long non-coding RNAs (lncRNAs) in tumorigenesis, we possess the aim to determine the action effects and mechanisms of LINC01002 in prostate cancer (PCa). Methods: Expression level of LINC01002, miR-650 or filamin A (FLNA) in PCa tissues and cells was assessed using quantitative real-time PCR (qPCR) or western blotting. Cell proliferative and migratory capacities were investigated by Cell Counting Kit-8 (CCK8) and wound healing assays. Cell apoptosis was investigated by the levels of Bax and Bcl-2. Xenograft models were constructed to testify the role of LINC01002 in vivo. The anticipated binding of miR-650 to LINC01002 or FLNA was confirmed by dual-luciferase reporter or RNA Binding Protein Immunoprecipitation (RIP) assays. Results: Relatively poor expression of LINC01002 and FLNA, and high expression of miR-650 were identified in PCa tumor specimens and cells. Ectopic LINC01002 expression restrained PCa cell proliferation/migration and provoked apoptosis in vitro, and blocked solid tumor growth in Xenograft models. MiR-650 was directly targeted by LINC01002, and it also directly bound to FLNA. MiR-650 reintroduction in PCa cells overexpressing LINC01002 or FLNA partly reversed the anti-cancer effects of LINC01002 or FLNA overexpression, thus recovering PCa cell proliferation/migration and repressing apoptosis. Conclusion: LINC01002 deregulation was linked to PCa development. LINC01002 exerted potential anti-cancer effects in PCa via targeting the miR-650/FLNA pathway, which, at least in part, provided a basis for the involvement of LINC01002 as a therapeutic target in PCa.