Knockdown of LncRNA SNHG14 regulates proliferation and apoptosis via activating miR-204-5p/HMGA1 axis in retinoblastoma

Abstract

Background: Retinoblastoma (RB) is an aggressive intraocular malignancy of infant and childhood, which seriously endangers the vision and life of children. Long non-coding RNA Small Nucleolar RNA Host Gene 14 (lncRNA SNHG14) as a novel oncogene is involved in the control of cancer cell progression. However, the effects and molecular mechanism of SNHG14 on retinoblastoma remain confusing.Methods: Levels of SNHG14, high mobility group protein A1 (HMGA1) mRNA and microRNA (miR)-204-5p were detected by quantitative real-time polymerase chain reaction. Cell proliferation and apoptosis were measured by CKK-8 assay or flow cytometry, respectively. Western blot was used to detect HMGA1 and apoptosis-related protein. The interaction between miR-204-5p and SNHG14 or HMGA1 was explored by luciferase reporter assay. Murine xenograft model was established using Y79 cells stably transfected with sh-SNHG14.Results: SNHG14 and HMGA1 were up-regulated in retinoblastoma tissues and cell lines, and knockdown of SNHG14 or HMGA1 suppressed cell proliferation and induced cell apoptosis in retinoblastoma. MiR-204-5p was confirmed to directly bind to SNHG14 and HMGA1, SNHG14 positively regulated HMGA1 expression via miR-204-5p. Importantly, the anti-tumor effects mediated by SNHG14 knockdown could be reversed by miR-204-5p inhibition or HMGA1 overexpression in retinoblastoma cells. Furthermore, xenograft model showed SNHG14 silence impeded tumor growth in vivo.Conclusion: Knockdown of SNHG14 suppressed retinoblastoma progression by regulating miR-204-5p/HMGA1 axis, revealing a potential target to develop appropriate treatment strategies for retinoblastoma.