The nuclear factor kappa B activation: the key step of cell proliferation in estrogen receptor-negative breast cancer cells / 中华外科杂志

<p><b>OBJECTIVE</b>To investigate the way of nuclear factor kappa B (NF-kappaB) activation and the mechanism of NF-kappaB-promoted proliferation in estrogen receptor (ER)-negative breast cancer cells.</p><p><b>METHODS</b>The protein of IkappaB kinase alpha (IKKalpha) was measured by Western blot and the influence on cell-cycle was assayed by flow cytometry (FCM).</p><p><b>RESULTS</b>The IKKalpha was tested higher in three ER-negative breast cancer cell lines than in MCF-7. The influence caused by epidermal growth factor (EGF), tumor necrosis factor (TNF)-alpha and E(2) to tumor cells' proliferation was tested. EGF could remarkably enhance cyclin D(1) expression about 83% more in EGF group than that in control group and proliferation index from 0.22 to 0.31 (P < 0.01). On the other hand, TNF-alpha inhibited cyclin D(1) expression. Protein kinase C inhibitor, Go6976, could peculiarly prevent NF-kappaB over-expression caused by EGF. The cell-cycle was assayed by FCM in phase G(0)/G(1) 69.36% and in phase S 22.77% when adding EGF and in phase G(0)/G(1) 91.54% and in phase S 7.81% when adding EGF and Go6976. The proliferation index decreased from 0.31 to 0.09 (P < 0.01).</p><p><b>CONCLUSIONS</b>EGF-EGFR pathway can provide ER-negative breast cancer cells the signal for the autonomous growth. This signal promoted tumor cells' proliferation is transmitted by activating NF-kappaB and expressing more cyclin D(1). In this pathway, NF-kappaB play an important role as signal transmitting. The strategy to NF-kappaB activating may provide new way to treat ER-negative breast cancers.</p>

Preliminary study on lymphocyte subsets of sentinel lymph nodes in breast cancer patients / 中华肿瘤杂志

<p><b>OBJECTIVE</b>To study the lymphocyte subsets of sentinel lymph nodes (SLN) in breast cancer patients.</p><p><b>METHODS</b>Flow cytometry was used to analyze the markers on the surface of lymphocytes such as CD3, CD4, CD8, CD16 and CD19 in the sentinel lymph node of breast cancer.</p><p><b>RESULTS</b>When lymph node metastasis did not occur, there was no significant difference in the number of CD3(+) T, CD4(+) T, CD8(+) T, CD16 NK and CD19 B cells between SLN cells and non-SLN cells. With lymph node metastasis, the proportion of CD4(+) and CD8(+) T cells was significantly changed, CD8(+) T cells (66.15 +/- 5.97) were the predominant cells instead of CD4(+) T cells (69.07 +/- 5.02), whereas no significant difference in CD3(+) T, CD16 NK and CD19 B cells.</p><p><b>CONCLUSION</b>The CD4(+) to CD8(+) T cell ratio in sentinel lymph nodes with metastasis is reversed in breast cancer patients. This might results from changes in microenvironment due to tumor cell invasion.</p>

Expression of tyrosine kinase Syk in breast cancer and their clinical significance / 中华外科杂志

<p><b>OBJECTIVE</b>To evaluate the effects of the Syk mRNA expression in human breast cancer on tumor growth and metastasis, and to study the correlation of expression of the Syk gene with ER, PR, p53 and HER2/neu.</p><p><b>METHODS</b>Specimens from 40 breast cancer patients (tumor tissues, adjacent normal tissues), 15 fibroadenoma were detected for their expression of the Syk gene and level of Syk mRNA by semi-RT-PCR technique. Meanwhile, ER, PR, p53, HER2/neu were detected in 40 tumor tissues from breast cancer with immunohistochemical staining.</p><p><b>RESULTS</b>All normal breast tissues were detected the expression of the Syk gene. Unlike normal breast tissue, 31 out of 40 breast cancer tissue did not show any detectable Syk mRNA expression, there were significant difference in two groups (chi(2) = 47.4, P < 0.05). The level of Syk mRNA in the primary breast cancer tissues were significantly lower than that in the adjacent non-cancerous breast tissues (t = 3.41, P < 0.05). Furthermore, only one breast cancer tissue in 18 patients with lymph node metastasis had the Syk mRNA expression, the rate and level of Syk mRNA expression in the patients with lymph node metastasis were lower than those without lymph node metastasis (chi(2) = 3.77, P < 0.05, t = 2.74, P < 0.05). Syk expression was correlated to p53 expression.</p><p><b>CONCLUSION</b>The expression of the Syk gene may play an important role in suppressing growth and metastasis of breast cancer.</p>

Optimal effects of liposome on antisense oligodeoxynucleotides uptake by mouse breast cancer TM40D cells and the effects of antisense oligodeoxynucleotides targeting c-erbB-2 on cell proliferation and apoptosis / 中华外科杂志

<p><b>OBJECTIVE</b>To study the optimal effects of liposome on antisense oligodeoxynucleotides targeting c-erbB-2 uptake by mouse breast cancer TM40D cells and effects of AS-ODNs on cell proliferation and apoptosis.</p><p><b>METHODS</b>Flow cytometric analysis and fluorescence microscope were used to study the transfection ratio of AS-ODNs in mouse breast cancer TM40D cells with/without liposome in 1, 2, 4, 6 hour and the distribution of AS-ODNs in cells. the effects of ODNs on cell proliferation and activation of apoptosis were examined by MTT assay and flow cytometry.</p><p><b>RESULTS</b>Liposome could promote AS-ODNs uptake by mouse breast cancer TM40D cells, flow cytometric analysis revealed that the time of the optimal effects was 4 hours and the percentage of FAM-positive cells reached 72.23%; the ratio maintained at a relatively high level at 6 h. Also liposome facilitated the entrance of AS-ODNs into nucleus. AS-ODNs restrained the proliferation of mouse breast cancer TM40D cells, and restraint rate was 50.24%. Meanwhile AS-ODNs promoted cell apoptosis. Flow cytometry analysis revealed that antisense ODNs increased cell apoptosis by 38.50%, compared with cultured cells group 9.13% and liposome group 9.29%.</p><p><b>CONCLUSIONS</b>Liposome could facilitate AS-ODNs to enter cells and their nucleus. AS-ODNs of C-erbB-2 restrained the proliferation of mouse breast cancer TM40D cells and promoted apoptosis.</p>

Expression of vascular endothelial cell growth factor and its receptor mRNA in breast cancer tissues / 中华外科杂志

<p><b>OBJECTIVE</b>To study the expression of vascular endothelial cell growth factor (VEGF) and its receptor FLT-1, FLK-1 mRNA in breast cancer tissues and their correlation with clinicopathological factors.</p><p><b>METHODS</b>The expression of VEGF and and its receptor FLT-1, FLK-1 mRNA were analyzed by reverse transcription - polymerase chain reaction (RT-PCR) in the specimens from 47 patients with breast cancer and 11 patients with benign breast disease.</p><p><b>RESULTS</b>VEGF121, 165 mRNA were all detected in malignant and benign breast tissues, with higher level, (0.420 +/- 0.133 and 0.291 +/- 0.094 respectively) in breast cancer tissues than in benign breast tissues, [0.196 +/- 0.067 (P = 0.000) and 0.206 +/- 0.058 (P = 0.001) respectively]. VEGF121 mRNA expression was stronger than VEGF165 mRNA expression (P = 0.000) in breast cancer tissues, whereas there is no significant difference in benign breast tissues (P = 0.666). FLT-1, FLK-1 mRNA were expressed in 18 of 47 (38.3%) and 12 of 47 (25.5%) breast cancer tissues respectively, but not in benign breast tissues. Moreover, no correlation was observed between the expression of VEGF121, VEGF165, FLT-1, FLK-1 mRNA in breast cancer tissues and patients' age, tumor size, lymph node metastasis, tumor stages, estrogen or progesterone receptor status.</p><p><b>CONCLUSION</b>The expression of VEGF and its receptor FLT-1, FLK-1 mRNA were up-regulated in breast cancer tissues, suggesting its important role in angiogenesis of breast cancer.</p>