Expression of HER-2 in MCF-7 breast cancer cells modulates anti-apoptotic proteins Survivin and Bcl-2 via the extracellular signal-related kinase (ERK) and phosphoinositide-3 kinase (PI3K) signalling pathways

Siddiqa, Aisha; Long, Linda M; Li, Liuxia; Marciniak, Robert A.; Kazhdan, Irene

doi:10.1186/1471-2407-8-129

Cited by 100 publications

(85 citation statements)

References 29 publications

(29 reference statements)

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“…Moreover, activated growth factor signaling can provide survival signals to protect from tamoxifenand fulvestrant-induced apoptosis (Kumar et al, 1996;Chung et al, 2002;Siddiqa et al, 2008). We show herein that ARTN-stimulated resistance to antiestrogen is mediated by upregulation of BCL-2 protein expression.…”

Section: Discussionsupporting

confidence: 50%

Artemin is estrogen regulated and mediates antiestrogen resistance in mammary carcinoma

et al. 2010

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We have previously identified an oncogenic role of artemin (ARTN), a member of glial cell derived neurotrophic factor family of ligands, in mammary carcinoma. We herein report that ARTN is an estrogen-inducible gene. Metaanalysis of gene expression data sets showed that ARTN expression is positively correlated to estrogen receptor (ER) status in human mammary carcinoma. Furthermore, in patients with ER-positive mammary carcinoma treated with tamoxifen, high ARTN expression is significantly correlated with decreased survival. Forced expression of ARTN in ER-positive human mammary carcinoma cells increased ER transcriptional activity, promoted estrogenindependent growth and produced resistance to tamoxifen and fulvestrant in vitro and to tamoxifen in xenograft models. ARTN-stimulated resistance to tamoxifen and fulvestrant is mediated by increased BCL-2 expression. Conversely, depletion of endogenous ARTN by smallinterfering RNA or functional antagonism of ARTN by antibody enhanced the efficacy of antiestrogens. Tamoxifen decreased ARTN expression in tamoxifen-sensitive mammary carcinoma cells whereas ARTN expression was increased in tamoxifen-resistant cells and not affected by tamoxifen treatment. Antibody inhibition of ARTN in tamoxifen-resistant cells improved tamoxifen sensitivity. Functional antagonism of ARTN therefore warrants consideration as an adjuvant therapy to enhance antiestrogen efficacy in ER-positive mammary carcinoma.

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Section: Discussionsupporting

confidence: 50%

Artemin is estrogen regulated and mediates antiestrogen resistance in mammary carcinoma

et al. 2010

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“…We focused on Bcl-xL and survivin, both of which are reported to be induced via phosphorylation of ERK pathway (33)(34)(35)(36)(37). We showed that CCL11 increased Bcl-xL and survivin expression in Ki-JK cells in vitro (Fig.…”

Section: Discussionmentioning

confidence: 99%

CCL11–CCR3 Interactions Promote Survival of Anaplastic Large Cell Lymphoma Cells via ERK1/2 Activation

et al. 2011

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CCR3 is a specific marker of anaplastic large cell lymphoma (ALCL) cells. ALCL cells also express CCL11, a ligand for CCR3, leading to the hypothesis that CCL11 may play an autocrine role in ALCL progression. In this study, we investigated a role of CCL11 in cell survival and growth of human Ki-JK cells, established from an ALCL patient, and murine EL-4 lymphoma cells. Both Ki-JK and EL-4 cells expressed cell surface CCR3. CCL11 increased cell survival rates of Ki-JK cells in a dose-dependent manner, whereas it promoted EL-4 cell proliferation. Furthermore, CCL11 induced phosphorylation of extracellular signal-regulated kinase (ERK) 1/ 2 in both Ki-JK cells and EL-4 cells. Cell survival and tumor proliferation promoted by CCL11 was completely blocked by inhibition of ERK phosphorylation. CCL11 induced expression of antiapoptotic proteins, Bcl-xL and survivin, in Ki-JK cells. CCL11 also enhanced tumor growth of EL-4 and Ki-JK cells in vivo. Consistent with these results, tumor cells of cutaneous ALCL expressed CCR3 and increased levels of phosphorylated ERK1/2, Bcl-xL, and survivin in situ. Thus, our findings prompt a novel therapeutic approach to treat relapses of an aggressive form of lymphoma based on the discovery that a cell surface marker of disease functions as a critical autocrine growth receptor. Cancer Res; 71(6); 2056-65. Ó2011 AACR.

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“…These molecular mechanism might be occurred by suppression of survivin protein expression through inhibition of its upstream protein, HER-2 and IKK. Inhibition of HER-2 and IKK could suppress the Pgp expression that correlated to resistance breast cancer cell induced by chemotherapeutic agent, doxorubicin (Siddiqa, et al, 2008;Gilmore, 2006).…”

Section: (A) (B) (C) (D) (E)mentioning

confidence: 99%

Brazilein Increased Cytotoxic Activity of Doxorubicin on MCF-7/DOX Cells

Laksmiani

Susidarti

Meiyanto

2017

IJCC

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Brazilein is a compound obtained in a large amount from the dried heartwood of Secang (Caesalpinia sappan L.). Brazilein has strong cytotoxic effect in several cancer cell lines. This research was designed to evaluate the cytotoxic effect of brazilein and its combination with a chemotherapy agent, doxorubicin on MCF-7/DOX breast cancer cells. In the cytotoxicity assay, MCF-7/DOX cells were cultured in the presence of brazilein solely and in combination with doxorubicin for 24 hours and cell viability was evaluated by using MTT assay. MTT assay showed a dose-dependent inhibition of cell proliferation with IC50 value of 37 µM. Brazilein increased doxorubicin's cytotoxic activity on MCF-7/DOX cells. Both of single treatment with different concentration of brazilein 12.5 and 25 M or doxorubicin 0.8 and 1 M gave cell viability percentage above 80%, but combination of them led to decrease the cell viability percentage significantly. Based on this research, it can be concluded that brazilein is potential to be developed as a co-chemotherapy agent on breast cancer cell that have been resistant to doxorubicin. Futher study must be held to evaluate its molecular mechanism.

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Expression of HER-2 in MCF-7 breast cancer cells modulates anti-apoptotic proteins Survivin and Bcl-2 via the extracellular signal-related kinase (ERK) and phosphoinositide-3 kinase (PI3K) signalling pathways

Cited by 100 publications

References 29 publications

Artemin is estrogen regulated and mediates antiestrogen resistance in mammary carcinoma

Artemin is estrogen regulated and mediates antiestrogen resistance in mammary carcinoma

CCL11–CCR3 Interactions Promote Survival of Anaplastic Large Cell Lymphoma Cells via ERK1/2 Activation

Brazilein Increased Cytotoxic Activity of Doxorubicin on MCF-7/DOX Cells

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