Journal
CANCER MANAGEMENT AND RESEARCH
Volume 13, Issue -, Pages 571-578Publisher
DOVE MEDICAL PRESS LTD
DOI: 10.2147/CMAR.S284258
Keywords
diffuse large B-cell lymphoma; SBF2-AS1; miR-494-3p; FGFR2; tumorigenesis
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This study revealed that SBF2-AS1 promoted the growth of DLBCL through the miR-494-3p/FGFR2 axis, and this mechanism was confirmed in in vivo tumorigenesis experiments.
Purpose: Currently, there is no efficient and feasible method for diffuse large B-cell lymphoma (DLBCL) in clinical practice, and the main reason is the unclear pathogenesis of DLBCL, which leads to a high fatality rate of DLBCL. Methods: Therefore, it is meaningful to explore the molecular mechanism of DLBCL and find a targeted therapeutic approach from the molecular level. Results: Long non-coding RNA (lncRNA) SBF2-AS1 was highly expressed in DLBCL tissues and cell lines. Silencing of SBF2-AS1 inhibited the viability and growth of OCI-LY-3 cells. Furthermore, SBF2-AS1 acted as a sponge of miR-494-3p and inhibited its expression. And miR-494-3p directly targeted FGFR2. Functionally, forced expression of miR-494-3p or knockdown of FGFR2 removed the promoted effects of lncRNA SBF2-AS1 on DLBCL development. In vivo tumorigenesis experiments indicated SBF2-AS1 accelerated tumor growth via miR-494-3p/FGFR2 axis. Conclusion: Our study revealed that SBF2-AS1 promoted the growth of DLBCL, which were mediated by miR-494-3p/FGFR2 axis.
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