长链非编码RNA SBF2-AS1通过海绵吸附miR-494-3p调控FGFR2促进弥漫性大B细胞淋巴瘤生长。

LncRNA SBF2-AS1 Promotes Diffuse Large B-Cell Lymphoma Growth by Regulating FGFR2 via Sponging miR-494-3p.

作者信息

Fu Dong-Wei, Liu Ai-Chun

机构信息

Department of Hematology, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang 150081, People's Republic of China.

出版信息

Cancer Manag Res. 2021 Jan 22;13:571-578. doi: 10.2147/CMAR.S284258. eCollection 2021.

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.

目的

目前在临床实践中，对于弥漫性大B细胞淋巴瘤（DLBCL）尚无有效且可行的方法，主要原因是DLBCL的发病机制尚不清楚，这导致DLBCL的死亡率很高。

方法

因此，探索DLBCL的分子机制并从分子水平找到靶向治疗方法具有重要意义。

结果

长链非编码RNA（lncRNA）SBF2-AS1在DLBCL组织和细胞系中高表达。沉默SBF2-AS1可抑制OCI-LY-3细胞的活力和生长。此外，SBF2-AS1作为miR-494-3p的海绵，抑制其表达。并且miR-494-3p直接靶向FGFR2。在功能上，强制表达miR-494-3p或敲低FGFR2可消除lncRNA SBF2-AS1对DLBCL发展的促进作用。体内肿瘤发生实验表明SBF2-AS1通过miR-494-3p/FGFR2轴加速肿瘤生长。