Research Paper Volume 13, Issue 15 pp 19306—19316

LncRNA-HAGLR motivates triple negative breast cancer progression by regulation of WNT2 via sponging miR-335-3p

HAGLR acted as a sponge of miR-335-3p and inhibited its expression. (A) MiRanda database showing the binding sites of miR-335-3p with HAGLR, and the mutant sequence of miR-335-3p. (B) Wild type and mutant miR-335-3p was transfected into HEK293 cells with or without HAGLR, and luciferase assay was to evaluate the binding between miR-335-3p and HAGLR. (C) BT549 cells were transfected with HAGLR plasmid or si-HAGLR or its NC, the mRNA level of miR-335-3p was detected using qRT-PCR. (D) The expression of miR-335-3p in para-carcinoma and cancer tissues was detected by qRT-PCR. (E) qRT-PCR analysis for miR-335-3p level in normal breast cell MCF10A and TNBC cell lines MDA-MB-231 and BT549. Data are mean ± SD; *P

Figure 3. HAGLR acted as a sponge of miR-335-3p and inhibited its expression. (A) MiRanda database showing the binding sites of miR-335-3p with HAGLR, and the mutant sequence of miR-335-3p. (B) Wild type and mutant miR-335-3p was transfected into HEK293 cells with or without HAGLR, and luciferase assay was to evaluate the binding between miR-335-3p and HAGLR. (C) BT549 cells were transfected with HAGLR plasmid or si-HAGLR or its NC, the mRNA level of miR-335-3p was detected using qRT-PCR. (D) The expression of miR-335-3p in para-carcinoma and cancer tissues was detected by qRT-PCR. (E) qRT-PCR analysis for miR-335-3p level in normal breast cell MCF10A and TNBC cell lines MDA-MB-231 and BT549. Data are mean ± SD; *P < 0.05, Abbreviation: ns: no statistical significance.