Breast cancer is considered as one of the multifactorial diseases. The aim of the current study is to investigate the association between P-cadherin and molecular subtypes of breast cancer, especially the basal-like subtype. Two hundred and thirteen breast-invasive ductal carcinomas were involved in this study. The expressions of P-cadherin were detected via immunohistochemistry. The 213 cases were divided into luminal A, luminal B, HER2 overexpression subtype, and normal breast-like and basal-like subtypes according to the standard of molecular breast cancer subtypes. In addition, the expressions of CK5/6 and CK14 were detected to distinguish between the normal breast-like and the basal-like subtypes. P-cadherin expression was found in 91 cases of 213 breast-invasive ductal carcinomas, with a positive rate of 42.7%. P-cadherin correlated negatively with estrogen receptor (ER) (p=0.001) and progesterone receptor (p=0.001), whereas it positively correlated with histologic grade (p=0.003), NPI (p=0.005), p53 (p=0.038), and Ki67 (p=0.022). P-cadherin expression showed a strong correlation with recurrence and distant metastasis (p=0.009), and invasion of the vascular and soft tissues (p=0.004). Moreover, P-cadherin expression existed in the basal-like and non-basal-like subtypes. During prognosis, P-cadherin expression was associated with decreased disease-free survival in patients (p=0.009) and overall survival (OS) (p=0.005). In addition, multivariate analysis showed that tumor grade (p=0.021), ER (p=0.015), clinical stage (p=0.001), and P-cadherin (p=0.033) were significant predictors of OS. The current data suggest that P-cadherin may be used to distinguish the basal-like subtype and to predict the outcome in view of the relationship with DFS and OS. Furthermore, P-cadherin expression may be useful in making treatment decisions.

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PurposeDYNLT3 is identified as an age‐related gene. Nevertheless, the specific mechanism of its carcinogenesis in breast tumor has not been clarified. This research aims to elucidate the role and the underlying molecular pathways of DYNLT3 on breast cancer tumorigenesis.MethodsThe differential expression of DYNLT3 among breast cancer, breast fibroids, and normal tissues, as well as in various breast cancer cell lines were detected by immunohistochemical staining, real‐time quantitative reverse transcription‐PCR and Western blotting, respectively. Additionally, the role of DYNLT3 on cell viability and proliferation were observed through cell counting kit‐8, bromodeoxyuridine, and colony formation experiments. Migratory and invasive abilities was envaulted by wound healing and Transwell methods. Apoptotic cells rate was examined by flow cytometry. Furthermore, nude mice xenograft models were established to confirm the role of DYNLT3 in tumor formation in vivo.ResultsDYNLT3 expression was highly rising in both breast cancer tissues and cells. DYNLT3 knockdown obviously suppressed cell growth, migration and invasion, and induced cell apoptosis in MDA‐MB‐231 and MCF‐7 breast cancer cells. The overexpression of DYNLT3 exerted the opposite effect in MDA‐MB‐231 cells. Moreover, DYNLT3 knockdown inhibited tumor formation in vivo. Mechanistically, an elevation of N‐cadherin and vimentin levels and a decline of E‐cadherin were observed when DYNLT3 was upregulated, which was reversed when DYNLT3 knockdown was performed.ConclusionDYNLT3 may function as a tumor‐promotor of age‐associated breast cancer, which is expected to provide experimental basis for new treatment options.