〔Abstract〕 To investigate the expression of Keratin 14 (KRT14) in Basal-like Breast Cancer (BLBC) and its biological functions and mechanisms . Methods The expression levels of KRT14 mRNA in BLBC and para- cancer breast tissues were analyzed using The Cancer Genome Atlas ( TCGA) database . qPCR , Western blot (WB) , and immunohistochemistry were employed to detect KRT14 expression in BLBC and adjacent normal tis- sues , and its correlation with clinicopathological features was analyzed . KRT14 overexpression and knockdown were performed in breast cancer cells , and cell scratch and transwell assays were performed to evaluate changes in migra- tion and invasion abilities . To investigate the expression of proteins related to the Wnt/β-catenin signaling pathway , including β-catenin ( catenin Beta 1) , Wnt1 ( wingless-type MMTV integration site family , member 1) , MMP7 ( matrix metallopeptidase 7) , and c-Myc (cellular myelocytomatosis viral oncogene homolog) , as well as the cellu- lar localization of β-catenin , WB and immunofluorescence (IF) techniques were employed . Additionally , a Wnt/ β-catenin signaling pathway inhibitor was used to verify the mechanism of action of KRT14 . Results The expres- sion of KRT14 was significantly higher in BLBC tissues compared to normal tissues (P < 0. 05) , and was associated with higher T stage , and histological grade( P < 0. 05) . The overexpression of KRT14 significantly enhanced the migration and invasion abilities of breast cancer cells , while the knockdown of KRT14 significantly reduced those a- bilities (P < 0. 01) . The overexpression of KRT14 can increase the expression levels of Wnt/β-catenin pathway-re- lated proteins β-catenin , Wnt1 , MMP7 , and c-Myc , thereby activating the Wnt/β-catenin pathway . Moreover , the inhibition of this pathway can eliminate the effects of KRT14 on cell migration and invasion . Conclusion The high expression of KRT14 in BLBC may promote the migration and invasion of breast cancer cells through the Wnt/β- catenin signaling pathway .