Enhancement of vascular endothelial growth factor–mediated angiogenesis in tamoxifen-resistant breast cancer cells: role of Pin1 overexpression

Kim, Mi Ra; Choi, Hong Seok; Yang, Jin Won; Park, Byung Chul; Kim, Jung-Ae; Kang, Keon Wook

doi:10.1158/1535-7163.mct-08-1061

Cited by 43 publications

(43 citation statements)

References 48 publications

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“…We showed that the Pin1 protein level was consistently increased in TAMR-MCF-7 cells compared to control MCF-7 cells (Kim et al, 2009a;2009b) (Fig. 1A).…”

Section: Transcriptional Activation Of the Pin1 Gene In Tamr-mcf-7 Cellsmentioning

confidence: 84%

“…Unfortunately, resistance to hormonal therapy is a major clinical problem -most cancer cells can utilize alternative mechanisms for growth and survival after initiation of first-line endocrine therapy (Ali et al, 2002). A series of our studies revealed that both VEGF-mediated angiogenesis and snail-dependent epithelial mesenchymal transitions were stimulated in TAMresistant breast cancer cells, and Pin1 overexpression in this cell type is a critical event for both processes (Kim et al, 2008;2009a;2009b). In the present study, we demonstrated that Pin1 overexpression in TAMR-MCF-7 cells was dependent on transcriptional activation of the Pin1 gene.…”

Section: Discussionmentioning

confidence: 94%

“…We previously demonstrated that VEGF production was increased via Pin1 up-regulation in TAMR-MCF-7 cells (Kim et al, 2009a). Hence, we determined the effect of LY294002 and SB203580 in VEGF secretion of TAMR-MCF-7 cells using VEGF-specific ELISA.…”

Section: Role Of Pi3k and P38 Kinase In E2f1-dependent Pin1 Expressiomentioning

confidence: 94%

“…The fractionated proteins were then transferred electrophoretically to nitrocellulose paper and immunoblotted with specific antibodies. Nuclear extracts were prepared as previously described (Kim et al, 2009a).…”

Section: Immunoblot Analysismentioning

confidence: 99%

“…We previously established TAM-resistant breast cancer cells using an ER-positive MCF-7 cell line (TAMR-MCF-7 cells) by long-term culture of MCF-7 cells in hormone-free culture medium that contained 4-hydroxytamoxifen (Choi et al, 2007). A series of our studies revealed that Pin1 was highly expressed in TAMR-MCF-7 cells and that it was required for both enhanced vascular endothelial growth factor (VEGF)-mediated angiogenesis and the Snail-dependent epithelial mesenchymal transition in the cell type (Kim et al, 2009a;2009b). These results suggested that Pin1 is a potential therapeutic target for the treatment of TAM-resistant breast cancer.…”

Section: Introductionmentioning

confidence: 97%

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PI3-Kinase/p38 Kinase-Dependent E2F1 Activation Is Critical for Pin1 Induction in Tamoxifen-Resistant Breast Cancer Cells

Lee

Nam

et al. 2011

Molecules and Cells

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“…We showed that the Pin1 protein level was consistently increased in TAMR-MCF-7 cells compared to control MCF-7 cells (Kim et al, 2009a;2009b) (Fig. 1A).…”

Section: Transcriptional Activation Of the Pin1 Gene In Tamr-mcf-7 Cellsmentioning

confidence: 84%

Section: Discussionmentioning

confidence: 94%

Section: Role Of Pi3k and P38 Kinase In E2f1-dependent Pin1 Expressiomentioning

confidence: 94%

Section: Immunoblot Analysismentioning

confidence: 99%

Section: Introductionmentioning

confidence: 97%

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PI3-Kinase/p38 Kinase-Dependent E2F1 Activation Is Critical for Pin1 Induction in Tamoxifen-Resistant Breast Cancer Cells

Lee

Nam

et al. 2011

Molecules and Cells

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AhR ligand aminoflavone suppresses α6‐integrin–Src–Akt signaling to attenuate tamoxifen resistance in breast cancer cells

Campbell

Mavingire

Khan

et al. 2018

Journal Cellular Physiology

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More than 40% of patients with luminal breast cancer treated with endocrine therapy agent tamoxifen demonstrate resistance. Emerging evidence suggests tumor initiating cells (TICs) and aberrant activation of Src and Akt signaling drive tamoxifen resistance and relapse. We previously demonstrated that aryl hydrocarbon receptor ligand aminoflavone (AF) inhibits the expression of TIC gene α6-integrin and disrupts mammospheres derived from tamoxifen-sensitive breast cancer cells. In the current study, we hypothesize that tamoxifen-resistant (TamR) cells exhibit higher levels of α6-integrin than tamoxifen-sensitive cells and that AF inhibits the growth of TamR cells by suppressing α6-integrin-Src-Akt signaling. In support of our hypothesis, TamR cells and associated mammospheres were found to exhibit elevated α6-integrin expression compared with their tamoxifen-sensitive counterparts. Furthermore, tumor sections from patients who relapsed on tamoxifen showed enhanced α6-integrin expression. Gene expression profiling from the TCGA database further revealed that basal-like breast cancer samples, known to be largely unresponsive to tamoxifen, demonstrated higher α6-integrin levels than luminal breast cancer samples. Importantly, AF reduced TamR cell viability and disrupted TamR mammospheres while concomitantly reducing α6-integrin messenger RNA and protein levels. In addition, AF and small interfering RNA against α6-integrin blocked tamoxifen-stimulated proliferation of TamR MCF-7 cells and further sensitized these cells to tamoxifen. Moreover, AF reduced Src and Akt signaling activation in TamR MCF-7 cells. Our findings suggest elevated α6-integrin expression is associated with tamoxifen resistance and AF suppresses α6-integrin-Src-Akt signaling activation to confer activity against TamR breast cancer.

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Inhibition of neointimal formation by trans‐resveratrol: Role of phosphatidyl inositol 3‐kinase‐dependent Nrf2 activation in heme oxygenase‐1 induction

Kim

Lim

Lee

et al. 2010

Molecular Nutrition Food Res

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Neointima, defined as abnormal growth of the intimal layer of blood vessels, is believed to be a critical event in the development of vascular occlusive disease. Although resveratrol's inhibitory effects on proliferation and migration of vascular smooth muscle cells has been reported, its activity on neointimal formation is still unclear. Oral administration of trans-resveratrol significantly suppressed intimal hyperplasia in a wire-injured femoral artery mouse model. In cultured vascular smooth muscle cells, trans-resveratrol inhibited platelet-derived growth factor-stimulated DNA synthesis and cell proliferation with down-regulation of cyclin D and pRB. Moreover, platelet-derived growth factor-induced production of reactive oxygen species was inhibited by trans-resveratrol and the compound induced heme oxygenase-1 (HO-1). The anti-proliferative activity of trans-resveratrol was reversed by an HO-1 inhibitor, ZnPPIX. Subcellular fractionation and reporter gene analyses revealed that trans-resveratrol increased the level of nuclear Nrf2 and antioxidant response element reporter activity, and that these were essential for the induction of HO-1. Trans-resveratrol also enhanced the activities of phosphatidyl inositol 3-kinase and extracellular signal regulated kinase, and phosphatidyl inositol 3-kinase was required for Nrf2/antioxidant response element-dependent HO-1 induction. These data have significant implications for the elucidation of the pharmacological mechanism by which trans-resveratrol prevents vascular occlusive diseases.

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Enhancement of vascular endothelial growth factor–mediated angiogenesis in tamoxifen-resistant breast cancer cells: role of Pin1 overexpression

Abstract: Acquired resistance to tamoxifen (TAM) is a serious therapeutic problem in breast cancer patients.

Cited by 43 publications

References 48 publications

PI3-Kinase/p38 Kinase-Dependent E2F1 Activation Is Critical for Pin1 Induction in Tamoxifen-Resistant Breast Cancer Cells

PI3-Kinase/p38 Kinase-Dependent E2F1 Activation Is Critical for Pin1 Induction in Tamoxifen-Resistant Breast Cancer Cells

AhR ligand aminoflavone suppresses α6‐integrin–Src–Akt signaling to attenuate tamoxifen resistance in breast cancer cells

Inhibition of neointimal formation by trans‐resveratrol: Role of phosphatidyl inositol 3‐kinase‐dependent Nrf2 activation in heme oxygenase‐1 induction

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