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Survivin expression is regulated by coexpression of human epidermal growth factor receptor 2 and epidermal growth factor receptor via phosphatidylinositol 3-kinase/AKT signaling pathway in breast cancer cells.
Cancer Res. 2005 Dec 01; 65(23):11018-25.CR

Abstract

Survivin, a member of the inhibitor of apoptosis protein family, is widely expressed in a variety of human cancer tissues. Survivin inhibits activation of caspases, and its overexpression can lead to resistance to apoptotic stimuli. In this study, survivin protein expression was assessed by immunohistochemical staining of 195 invasive breast cancer specimens. Overall, 79.5% of the tumors were positive for survivin. The expression of epidermal growth factor receptor (EGFR) family, human epidermal growth factor receptor 2 (HER2) and EGFR, was also examined in 53 cases, and consequently, it was indicated that survivin positivity might be correlated with the coexpression of HER2 and EGFR. To clarify the regulatory mechanism of survivin expression in breast cancer cells, the effect of HER2 and/or EGFR expression on the survivin levels was examined. It was revealed that the survivin protein level was up-regulated by the coexpression of HER2 and EGFR, leading to the increased resistance against etoposide-induced apoptosis in breast cancer cells. Conversely, survivin levels and apoptosis resistance were decreased when cells were treated with HER2-specific inhibitor, Herceptin. Although Herceptin could down-regulate both phosphatidylinositol 3-kinase (PI3K)/AKT signal and mitogen-activated protein/extracellular signal-related kinase (ERK) kinase 1 (MEK1)/ERK signal in HER2-positive breast cancer cells, PI3K-specific inhibitor but not MEK1-specific inhibitor could decrease the survivin levels. The present study clarified the regulatory mechanism of HER2 in the expression of survivin protein in breast cancer cells.

Authors+Show Affiliations

Department of Pathology, Sapporo Medical University School of Medicine, Chuo-ku, Sapporo, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16322251

Citation

Asanuma, Hiroko, et al. "Survivin Expression Is Regulated By Coexpression of Human Epidermal Growth Factor Receptor 2 and Epidermal Growth Factor Receptor Via Phosphatidylinositol 3-kinase/AKT Signaling Pathway in Breast Cancer Cells." Cancer Research, vol. 65, no. 23, 2005, pp. 11018-25.
Asanuma H, Torigoe T, Kamiguchi K, et al. Survivin expression is regulated by coexpression of human epidermal growth factor receptor 2 and epidermal growth factor receptor via phosphatidylinositol 3-kinase/AKT signaling pathway in breast cancer cells. Cancer Res. 2005;65(23):11018-25.
Asanuma, H., Torigoe, T., Kamiguchi, K., Hirohashi, Y., Ohmura, T., Hirata, K., Sato, M., & Sato, N. (2005). Survivin expression is regulated by coexpression of human epidermal growth factor receptor 2 and epidermal growth factor receptor via phosphatidylinositol 3-kinase/AKT signaling pathway in breast cancer cells. Cancer Research, 65(23), 11018-25.
Asanuma H, et al. Survivin Expression Is Regulated By Coexpression of Human Epidermal Growth Factor Receptor 2 and Epidermal Growth Factor Receptor Via Phosphatidylinositol 3-kinase/AKT Signaling Pathway in Breast Cancer Cells. Cancer Res. 2005 Dec 1;65(23):11018-25. PubMed PMID: 16322251.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Survivin expression is regulated by coexpression of human epidermal growth factor receptor 2 and epidermal growth factor receptor via phosphatidylinositol 3-kinase/AKT signaling pathway in breast cancer cells. AU - Asanuma,Hiroko, AU - Torigoe,Toshihiko, AU - Kamiguchi,Kenjiro, AU - Hirohashi,Yoshihiko, AU - Ohmura,Tousei, AU - Hirata,Koichi, AU - Sato,Masaaki, AU - Sato,Noriyuki, PY - 2005/12/3/pubmed PY - 2006/1/26/medline PY - 2005/12/3/entrez SP - 11018 EP - 25 JF - Cancer research JO - Cancer Res VL - 65 IS - 23 N2 - Survivin, a member of the inhibitor of apoptosis protein family, is widely expressed in a variety of human cancer tissues. Survivin inhibits activation of caspases, and its overexpression can lead to resistance to apoptotic stimuli. In this study, survivin protein expression was assessed by immunohistochemical staining of 195 invasive breast cancer specimens. Overall, 79.5% of the tumors were positive for survivin. The expression of epidermal growth factor receptor (EGFR) family, human epidermal growth factor receptor 2 (HER2) and EGFR, was also examined in 53 cases, and consequently, it was indicated that survivin positivity might be correlated with the coexpression of HER2 and EGFR. To clarify the regulatory mechanism of survivin expression in breast cancer cells, the effect of HER2 and/or EGFR expression on the survivin levels was examined. It was revealed that the survivin protein level was up-regulated by the coexpression of HER2 and EGFR, leading to the increased resistance against etoposide-induced apoptosis in breast cancer cells. Conversely, survivin levels and apoptosis resistance were decreased when cells were treated with HER2-specific inhibitor, Herceptin. Although Herceptin could down-regulate both phosphatidylinositol 3-kinase (PI3K)/AKT signal and mitogen-activated protein/extracellular signal-related kinase (ERK) kinase 1 (MEK1)/ERK signal in HER2-positive breast cancer cells, PI3K-specific inhibitor but not MEK1-specific inhibitor could decrease the survivin levels. The present study clarified the regulatory mechanism of HER2 in the expression of survivin protein in breast cancer cells. SN - 0008-5472 UR - https://www.unboundmedicine.com/medline/citation/16322251/Survivin_expression_is_regulated_by_coexpression_of_human_epidermal_growth_factor_receptor_2_and_epidermal_growth_factor_receptor_via_phosphatidylinositol_3_kinase/AKT_signaling_pathway_in_breast_cancer_cells_ L2 - http://cancerres.aacrjournals.org/cgi/pmidlookup?view=long&pmid=16322251 DB - PRIME DP - Unbound Medicine ER -