目的:探讨Linc00339对三阴乳腺癌发生发展的作用及其相关分子机制。方法:采用实时荧光定量PCR(qRT-PCR)法检测人乳腺正常上皮细胞和乳腺癌细胞中Linc00339的表达水平；采用质粒转染试验在MDA-MB-231细胞中过表达Linc00339；采用四甲基偶氮唑盐(MTT)法检测MDA-MB-231细胞的活性；采用黏附试验、Transwell试验分别检测MDA-MB-231细胞的黏附、侵袭和迁移能力；采用Western blot检测MDA-MB-231细胞中APC、Wnt/β-catenin信号通路相关蛋白的表达水平；采用qRT-PCR法检测MDA-MB-231细胞中miRNA-135a、miRNA-135b及miRNA-138的表达水平；将体外转染成功的MDA-MB-231细胞接种于裸鼠体内建立荷瘤裸鼠模型，观察和测量肿瘤块的体积和重量，采用Western blot检测裸鼠瘤体组织中APC、Wnt/β-catenin信号通路相关蛋白的表达水平，采用qRT-PCR法检测裸鼠瘤体组织中miRNA-135a、miRNA-135b及miRNA-138的表达水平。结果:与乳腺正常上皮细胞组(Hs578Bst)相比，乳腺癌细胞组(MCF-7、MDA-MB-468、MDA-MB-231)的Linc00339表达水平均显著上调，以三阴乳腺癌MDA-MB-231细胞尤为显著；转染实验结果表明与pcDNA3.1组相比，Linc00339转染显著上调Linc00339表达水平并可显著增加MDA-MB-231细胞的活力；Linc00339过表达能够显著增加MDA-MB-231细胞的增殖、黏附、迁移和侵袭能力，增加荷瘤裸鼠肿瘤块的体积和重量；Western blot结果均表明体内外Linc00339过表达能够下调APC蛋白的表达和上调Wnt/β-catenin信号蛋白的表达，同时qRT-PCR结果表明Linc00339过表达能够上调miRNA-135b表达水平，而对miRNA-135a和miRNA-138无影响。结论:Linc00339可能通过miR-135b/APC介导的Wnt/β-catenin信号通路促进三阴乳腺癌的发生和发展。“,”Objective:To investigate the role of Linc00339 in the development of triple-negative breast cancer and its related molecular mechanisms.Methods:The expression levels of Linc00339 in human normal breast epithelial cells and breast cancer cells were detected by real time fluorescent quantitative polymerase chain reaction (qRT-PCR). The Linc00339 was overexpressed in MDA-MB-231 cells by plasmid transfection test; the activity of MDA-MB-231 cells was detected by methyl thiazolyl tetrazolium (MTT) method; the adhesion, invasion and migration ability of MDA-MB-231 cells were detected by adhesion test and transwell test respectively; Western blot was used to detect the expression of APC and Wnt/β-catenin signaling pathway-related proteins in MDA-MB-231 cells. qRT-PCR was used to detect the expression of miRNA-135a, miRNA-135b and miRNA-138 in MDA-MB-231 cells. MDA-MB-231 cells were successfully transfected into nude mice to establish tumor-bearing nude mice model. The volume and weight of tumor were observed and measured. The expression levels of APC, Wnt/β - catenin signaling pathway related proteins were detected by Western blot, and the expression levels of miRNA-135a, miRNA-135b and miRNA-138 were detected by qRT-PCR.Results:Compared with the normal breast epithelial cell group (Hs578Bst), the expression level of Linc00339 in breast cancer cell lines (MCF-7, MDA-MB-468, MDA-MB-231) was significantly up-regulated, especially MDA-MB-231. The results of transfection experiments showed that the expression level of Linc00339 and cell viability were significantly up-regulated in the Linc00339 group compared with the pcDNA3.1 group. The overexpression of Linc00339 significantly increased the proliferation, adhesion and migration and invasion ability of MDA-MB-231 cells, as well as increased the volume and weight of tumor mass in tumor-bearing nude mice. Western blot results showed that Linc00339 overexpression can down-regulate APC protein expression and up-regulate Wnt/β-catenin signaling protein expression. Meanwhile, qRT-PCR results indicated Linc00339 overexpression can up-regulate miRNA-135b expression levels without affecting miRNA-135a and miRNA-138.Conclusions:This study demonstrated that Linc00339 may promote the development and progression of triple-negative breast cancer via the miR-135b/APC-mediated Wnt/β-catenin signaling pathway.