RESUMO
Objective To observe the levels of serum VEGF in different molecular subtypes of breast cancer and explore its relationship with response to neoadjuvant chemotherapy. Methods Levels of serum VEGF in 110 cases with breast cancer underwent neoadjuvant chemotherapy were detected by ELISA prior to and after 3 cycles of neoadjuvant chemotherapy. Clinical response to neoadjuvant chemotherapy was evaluated by physical examination and ultrasonography. Results Levels of serum VEGF were significantly increased in breast cancer patients with≥4 lymph node metastasis than those with < 4 lymph node[(307.31 ± 101.42) pg/mL vs. (170.16 ± 73.07) pg/mL,P = 0.017]. Patients with positive HER-2 status had significantly higher levels of serum VEGF than those with HER-2 negative status [(235.15 ± 88.42 ) pg/mL vs. (179.82 ± 69.90) pg/mL, P = 0.024]. No significant difference was observed among age , menopausal status and hormone status. In patients with neoadjuvant chemotherapy of cCR and Cpr,the mean levels of serum VEGF were (205.75 ± 78.12) pg/mL and (226.04 ± 89.04) pg/mL, respectively. After 3 cycles of chemotherapy, levels of serum VEGF decreased to (145.15 ± 67.08) pg/mL and (161.27 ± 93.57) pg/mL. There was significant difference between two groups (P=0.009,0.014). In patients with SD or PD response, no significant difference was observed between levels of serum VEGF before and after chemotherapy (P = 0.577). Conclusions Levels of serum VEGF in breast cancer correlate with lymph nodes metastasis and HER-2 status and may decrease after neoadjuvant chemotherapy. However,whether or not the levels of serum VEGF can be used as a biomarker for response to neoadjuvant chemotherapy needs more further studies.
RESUMO
Objective To investigate the effects of Mus81 gene silencing on the chemosensitivity of human colon cancer HCT116 cells to oxaliplatin and explore the underlying mechanisms. Methods lentiviral-mediated RNAi was employed to inhibit Mus81 gene in human colon cancer HCT116 cells. MTT assay was employed to evaluate oxaliplatin chemosensitivity of HCT116. Cell apoptosis rate was detected by Annexin V-APC staining and the expression levels of p53, while Bax and Bcl-2 in HCT116 cells were detected by Real-time PCR and Western blot. Results Oxaliplatin IC50 of Mus81 depleted HCT116 cells was significantly decreased. After oxaliplatin treatment, the cell apoptosis rate of Mus81 silenced HCT116 cells was increased by 77.6% (P < 0.05), and the expression of p53 and Bax in these cells was obviously increased but the expression of Bcl-2 was significantly decreased (P < 0.01). Introducing Mus81 gene in Mus81 depleted HCT116 cells could reduce apoptosis rate. Conclusion Mus81 gene silencing can significantly improve oxliplatin chemosensitivity of HCT116 cells possibly by promoting cell apoptosis through regulating the expression of p53, Bax and Bcl-2.