Abstract
Breast cancer (BC) represents the most commonly diagnosed malignancy among women. Long non-coding RNAs (lncRNAs) can be transferred by extracellular vesicles (EVs) to participate in BC progression. This study demonstrated that SNHG16 expression was significantly increased in BC tissues and cells. Overexpression of SNHG16 promoted the migration, invasion, and epithelial–mesenchymal transition (EMT) of BC cells. SNHG16 was carried by EVs. Bioinformatics analysis predicted that SNHG16 regulated PPAPDC1A expression by sponging miR-892b, which was confirmed by RNA-fluorescence in situ hybridization (FISH), RT-qPCR, dual-luciferase gene reporter assay, and RNA immunoprecipitation (RIP). MDA-MB-157 and HS578T cells were transfected with pcDNA3.1-SNHG16, miR-892b-mimic, or si-PPAPDC1A for functional rescue experiments in vitro, and the cells were treated with MDA-MB-231 cell-derived EVs. The results confirmed that enhanced miR-892b expression partially eliminated the increase of migration, invasion, and EMT of BC cells mediated by SNHG16 or EVs. The lung metastasis model in nude mice was established by injecting HS578T cells via tail vein. The results showed that si-SNHG16 reduced the metastatic nodules and decreased the vimentin expression. In conclusion, EVs derived from BC cells transferred SNHG16 via the miR-892b/PPAPDC1A axis, thus promoting EMT, migration, and invasion of BC.
Highlights
As the most commonly diagnosed malignancy in women (Libson and Lippman, 2014), breast cancer (BC) initiation is attributed to multiple risk factors, such as DNA damage and genetic alteration (Akram et al, 2017)
To explore the role of SNHG16 in Breast cancer (BC), we screened the differential expression of SNHG16 in BC samples and normal samples collected by TCGA and GTEX databases, and found that SNHG16 expression in BC samples was notably promoted (Figure 1A)
This study demonstrated that BC-cell Extracellular vesicles (EVs) promoted BC metastasis by carrying Long non-coding RNAs (lncRNAs) SNHG16 via the miR-892b/PPAPDC1A axis (Figure 8)
Summary
As the most commonly diagnosed malignancy in women (Libson and Lippman, 2014), breast cancer (BC) initiation is attributed to multiple risk factors, such as DNA damage and genetic alteration (Akram et al, 2017). The current therapeutic strategies available for BC patients include hormone therapy, radiotherapy, surgery, and chemotherapy (Akram et al, 2017). Extracellular vesicles (EVs) are cell-derived microparticles that exist in body fluids, including microbubbles, exosomes, and apoptotic bodies (Sun et al, 2018). BC cell-derived EVs are reported to facilitate cancer cell proliferation and oncogene amplification (Keklikoglou et al, 2019). EVs promote the processes conducive to cancer progression, such as extracellular matrix remodeling, angiogenesis induction, and pre-metastasis niche initiation (Wang and Gires, 2019; Kalluri, 2016). The potential participation of EVs in the progression of BC metastasis is poorly understood
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