ABSTRACT
Background and purpose: Factor that binds to the inducer of short transcripts of human immuno-deficiency virus-1 (FBI-1) in a variety of malignant tumors showed high expression levels, which may be closely related to tumor proliferation and differentiation, angiogenesis, metastasis, but its relationship with breast cancer has not been fully elucidated. The purpose of this study was to investigate the expression of FBI-1 in breast cancer cells, and to study the effect of FBI-1 gene expression on the proliferation of breast cancer cells and its possible mechanism. Methods:Real-time fluorescent quantitative polymerase chain reaction (RTFQ-PCR) and Western blot analysis were applied to detect FBI-1 expression in normal human mammary epithelial cell line MCF-10A and breast cancer cell MCF-7. RNA interference method was used to down-regulate FBI-1 expression in MCF-7 cells. The cell proliferation was measured by CCK-8 kit and colony formation assay. RTFQ-PCR and Western blot were used to detect the expression of FBI-1 and NF-κBp65 in MCF-7 cells before and after the interference of FBI-1 expression. Results: The expression of FBI-1 was higher in breast cancer cells than that in normal human mammary epithelial cells (P<0.05). The effects of FBI-1 down-regulation inhibited proliferation in MCF-7 cells (P<0.05). At the same time, after inhibition of FBI-1, the NF-κBp65 mRNA and protein expression levels were significantly decreased (P<0.05). Conclusion: FBI-1 is highly expressed in breast cancer cells. Down-regulated FBI-1 expression can inhibit the proliferation of breast cancer cells,and its mechanism may be related to the inhibition of NF-κB signaling pathway.
ABSTRACT
<p><b>BACKGROUND</b>This study was designed in an attempt to determine the influence of neoadjuvant chemotherapy on estrogen receptor (ER), progesterone receptor (PR), human epidermal growth factor receptor 2 (Her-2), and Ki-67 expressions in patients with breast cancer.</p><p><b>METHODS</b>Pre- and post-neoadjuvant chemotherapy, paired-tumor specimens from 103 patients with breast cancer administrated with anthracycline or anthracycline combined taxane regimen were collected. Immunohistochemical staining for ER, PR, Her-2, and Ki-67 was performed by the DAKO EnVision method.</p><p><b>RESULTS</b>Among the 103 cases, five patients (4.9%) had a complete response (CR), 82 (79.6%) partial response (PR), 15 (14.6%) stable disease (SD), and one (0.9%) progressive disease (PD), yielding an overall response rate (CR + PR) of 84.5%. Nine patients achieved pathological CR. There was a significant decrease in the average index of Ki-67 postneoadjuvant chemotherapy, compared with that before chemotherapy (24.1% vs. 39.7%, P < 0.001). After neoadjuvant chemotherapy, the changes of Ki-67 in different subtypes of breast cancer were different (P < 0.001), and these changes correlated with response to neoadjuvant chemotherapy (P < 0.001). No significant changes in immunohistochemical expression were observed for ER, PR and Her-2.</p><p><b>CONCLUSIONS</b>Neoadjuvant chemotherapy apparently reduced Ki-67 index in primary breast carcinomas, but profiles for ER, PR and Her-2 were not significantly different before and after neoadjuvant chemotherapy. The change of Ki-67 correlated with molecular subtypes and response to neoadjuvant chemotherapy, suggesting that Ki-67 index was a surrogate marker to predict the treatment response of neoadjuvant chemotherapy.</p>