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- Title
LINC01002 Targets miR-650/FLNA Pathway to Suppress Prostate Cancer Progression.
- Authors
Qian, Li; Wang, Yue; Xiong, Yuzhen; Ren, Hetian; Liu, Shili; Chen, Dandan; Liu, Yang
- Abstract
Introduction: In view of the vital implication of long noncoding RNAs 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 or Western blotting. Cell proliferative and migratory capacities were investigated by Cell Counting Kit-8 (CCK-8) 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 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 anticancer 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 anticancer 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.
- Subjects
BINDING site assay; PROSTATE cancer; CANCER invasiveness; RNA-binding proteins; LINCRNA; SYNCRIP protein; ANDROGEN receptors
- Publication
Urologia Internationalis, 2023, Vol 107, Issue 5, p526
- ISSN
0042-1138
- Publication type
Article
- DOI
10.1159/000529947