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[The nuclear factor kappa B activation: the key step of cell proliferation in estrogen receptor-negative breast cancer cells].
Zhonghua Wai Ke Za Zhi. 2005 Aug 01; 43(15):1014-6.ZW

Abstract

OBJECTIVE

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.

METHODS

The protein of IkappaB kinase alpha (IKKalpha) was measured by Western blot and the influence on cell-cycle was assayed by flow cytometry (FCM).

RESULTS

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).

CONCLUSIONS

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.

Authors+Show Affiliations

Department of General Surgery, the First Affiliated Hospital, Nanjing Medical University, Nanjing 210029, China. whj_888@sohu.comNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

English Abstract
Journal Article

Language

chi

PubMed ID

16194364

Citation

Wang, Han-jin, et al. "[The Nuclear Factor Kappa B Activation: the Key Step of Cell Proliferation in Estrogen Receptor-negative Breast Cancer Cells]." Zhonghua Wai Ke Za Zhi [Chinese Journal of Surgery], vol. 43, no. 15, 2005, pp. 1014-6.
Wang HJ, Wu ZY, Fan P, et al. [The nuclear factor kappa B activation: the key step of cell proliferation in estrogen receptor-negative breast cancer cells]. Zhonghua Wai Ke Za Zhi. 2005;43(15):1014-6.
Wang, H. J., Wu, Z. Y., Fan, P., & Bian, J. M. (2005). [The nuclear factor kappa B activation: the key step of cell proliferation in estrogen receptor-negative breast cancer cells]. Zhonghua Wai Ke Za Zhi [Chinese Journal of Surgery], 43(15), 1014-6.
Wang HJ, et al. [The Nuclear Factor Kappa B Activation: the Key Step of Cell Proliferation in Estrogen Receptor-negative Breast Cancer Cells]. Zhonghua Wai Ke Za Zhi. 2005 Aug 1;43(15):1014-6. PubMed PMID: 16194364.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - [The nuclear factor kappa B activation: the key step of cell proliferation in estrogen receptor-negative breast cancer cells]. AU - Wang,Han-jin, AU - Wu,Zheng-yan, AU - Fan,Ping, AU - Bian,Jian-min, PY - 2005/10/1/pubmed PY - 2007/3/17/medline PY - 2005/10/1/entrez SP - 1014 EP - 6 JF - Zhonghua wai ke za zhi [Chinese journal of surgery] JO - Zhonghua Wai Ke Za Zhi VL - 43 IS - 15 N2 - OBJECTIVE: 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. METHODS: The protein of IkappaB kinase alpha (IKKalpha) was measured by Western blot and the influence on cell-cycle was assayed by flow cytometry (FCM). RESULTS: 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). CONCLUSIONS: 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. SN - 0529-5815 UR - https://www.unboundmedicine.com/medline/citation/16194364/[The_nuclear_factor_kappa_B_activation:_the_key_step_of_cell_proliferation_in_estrogen_receptor_negative_breast_cancer_cells]_ L2 - http://journal.yiigle.com/LinkIn.do?linkin_type=pubmed&amp;issn=0529-5815&amp;year=2005&amp;vol=43&amp;issue=15&amp;fpage=1014 DB - PRIME DP - Unbound Medicine ER -