RESUMO
Kinesin Family Member 3A (KIF3A) was recognized as a key factor of ciliogenesis and transport system of primary cilia in normal cells. However, its possible function on cancer cells has yet to be identified. In the present study, microarray tissue chips, including 230 breast cancer samples, were applied to determine the KIF3A expression pattern by immunological histological chemistry. Statistical analysis on the KIF3A expression level and the currently used clinicopathological characteristics of breast cancer patients was carried out. Follow-up data of these patients over 10 years were also used to evaluate the relationship between KIF3A and the survival rate. The expression levels of KIF3A were significantly higher in 140 breast cancer tissues than those of 90 para-carcinoma samples, which served as controls (P<0.001). In addition, in a further 70 paired samples, the same higher expression level was observed in cancer tissues compared with their self-paired controls (P<0.001). Furthermore, the high expression of KIF3A in breast cancer tissue correlated with the status of estrogen receptor, androgen receptor, epidermal growth factor receptor and Ki-67 of breast cancer patients, and were also related to their pathology grade and lymph node metastasis. The survival analysis showed a better survival rate in the patients with a higher expression level of KIF3A. Collectively, the triadic associations of KIF3A, the currently used clinicopathological parameters and survival rate suggest that KIF3A is involved in the tumorigenesis and progression of breast cancer. Thus, KIF3A could be considered a promising novel prognostic index in breast cancer.
RESUMO
It is not well established whether miR-93 is involved in drug resistance and epithelial-mesenchymal transition (EMT) in breast cancer, and its underlying mechanism remains uncertain. In the present study, the expression differences of miR-93 between paired breast cancer tissues confirmed it is involved in the progression of breast cancer. Such a difference was also observed in doxorubicin-resistant and -sensitive cells. Overexpressed miR-93 in sensitive cells revealed increases in cellular proliferation and the expression levels of drug-resistant-related genes, and a decrease in sensitivity to doxorubicin. This demonstrated the relationship between miR-93 and breast cancer drug resistance. Simultaneously, EMT was confirmed in miR-93 overexpressing sensitive cells. This indicated the triadic relationship among miR-93, EMT and drug resistance in breast cancer. We applied the Dual-luciferase Reporter assay to expose the direct interaction between miR-93 and PTEN, which suggested that miR-93 contributes to inducing EMT and drug resistance of breast cancer cells by targeting PTEN.
