Purpose: To investigate the effects of lncRNA RHPN1-AS1 on retinoblastoma (RB) and further explore its underlying molecular mechanisms.
Methods: The expression of RHPN1-AS1, miR-3133, (JAK2), and signal transducer and activator of transcription 3 (STAT3) was detected by qRT-PCR. CCK-8, EDU, and flow cytometry assays were conducted to assess the proliferation activity and apoptosis of RB cells. Double fluorescein and RNA immunoprecipitation assays were performed to detect the interaction between RHPN1-AS1 and miR-3133 or miR-3133 and JAK2. Western blotting was performed to detect the expression of apoptosis-related proteins.
Results: In RB cells, RHPN1-AS1 was upregulated. Silencing RHPN1-AS1 inhibited the activity of RB cells and promoted apoptosis. The expressions of proapoptotic factors (Bax and p53) were increased, while antiapoptotic factors (Bcl-2 and Survivin) were suppressed in siRHPN1-AS1 groups. Furthermore, we predicted and verified that RHPN1-AS1 regulated RB progression by targeting miR-3133/JAK2. In addition, siRHPN1-AS1 also inhibited oncogene STAT3 protein expression.
Conclusion: lncRNA RHPN1-AS1 served as a sponge for miR-3133 to counteract miR-3133-mediated JAK2/STAT3 suppression, indicating that the lncRNA RHPN1-AS1 may be a potential therapeutic target for the treatment of RB.
Copyright © 2020 Zhao-Na Li et al.