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

• Published in: Aging (Albany, NY.) NY.), 2021-08, Vol.13 (15), p.19306-19316
• Main Authors: Jin, Liting, Luo, Chenggang, Wu, Xinhong, Li, Manxiu, Wu, Shun, Feng, Yaojun
• Format: Article
• Language: English
• Subjects: Animals; Carcinogenesis - genetics; Cell Line, Tumor; Cell Proliferation; Gene Expression Regulation, Neoplastic; Humans; Mice; Mice, Nude; MicroRNAs - genetics; MicroRNAs - metabolism; Research Paper; RNA, Long Noncoding - genetics; Triple Negative Breast Neoplasms - genetics; Triple Negative Breast Neoplasms - metabolism; Wnt2 Protein - genetics; Wnt2 Protein - metabolism; Xenograft Model Antitumor Assays
• ISSN: 1945-4589; 1945-4589
• DOI: 10.18632/aging.203272

Triple negative breast cancer (TNBC) is a group of highly heterogeneous mixed breast cancer at the level of gene expression profile. Therefore, it is of great clinical significance to explore the molecular mechanism of TNBC and find a targeted therapeutic approach from the molecular level. Long non-coding RNA (lncRNA) HAGLR expression level was measured by and qRT-PCR in TNBC tissues and cell lines. EdU, MTT, wound healing and Transwell assays were performed to explore the role of HAGLR on the malignancy of TNBC cells. Luciferase assay was used to clarify the binding between miR-335-3p with HAGLR and WNT2. The tumor formation experiment in nude mice was used to explore the function of HAGLR . HAGLR was increased in TNBC tissues and cell lines. Silencing of HAGLR inhibited viability, proliferation, migration, and invasion of BT549 cells. Furthermore, HAGLR acted as a sponge of miR-335-3p and inhibited its expression. And miR-335-3p directly targeted WNT2. Functionally, forced expression of miR-335-3p or knockdown of WNT2 removed the promoted effects of lncRNA HAGLR on TNBC development. tumorigenesis experiments indicated HAGLR accelerated tumor growth via miR-335-3p/WNT2 axis. Our study revealed that HAGLR promoted the growth of TNBC, which was mediated by miR-335-3p/WNT2 axis.