Recently, long noncoding RNAs (lncRNAs) have become the key gene regulators and 
prognostic biomarkers in various cancers. Through microarray data, Linc00339 was 
identified as a candidate oncogenic lncRNA. We compared the expression levels of 
Linc00339 in several breast cancer cell lines and normal mammary gland 
epithelial cell line. The effects of Linc00339 on tumor progression were 
examined both in vitro and in vivo. 
3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assays were applied 
to evaluate the functions of Linc00339, miR-377-3p, and HOXC6 on cell 
proliferation. Flow cytometry analysis was used to detect apoptosis and cell 
cycle distribution. Overall survival (OS) was analyzed using data from The 
Cancer Genome Atlas and molecular taxonomy of breast cancer international 
consortium (METABRIC). Dual luciferase assay and RNA immunoprecipitation were 
performed to confirm the interaction between Linc003339 and miR-377-3p. 
Linc00339 was increased in breast cancer cell lines compared with the normal 
epithelial cell. Through in vitro and in vivo experiments, Linc00339 
overexpression promoted triple-negative breast cancer (TNBC) proliferation, 
inhibited cell cycle arrest, and suppressed apoptosis. Silencing of Linc00339 
obtained the opposite effects. Mechanistic investigations demonstrated that 
Linc00339 could sponge miR-377-3p and regulate its expression. Higher expression 
of miR-377-3p indicated longer OS in breast cancer patients, especially in TNBC 
patients. Overexpression of miR-377-3p retarded TNBC cell growth through 
regulating cell cycle distribution and apoptosis. And miR-377-3p was involved in 
Linc00339-mediated TNBC proliferation through regulating HOXC6 expression. 
Knockdown of HOXC6 inhibited TNBC progression. In conclusion, our results 
illuminated that the novel Linc00339/miR-377-3p/HOXC6 axis played a critical 
role in TNBC progression and might be a promising therapeutic target for TNBC 
treatment.