Proliferation of Breast Cancer Cells: Regulation, Mediators, Targets for Therapy

Mešter, Ján; Redeuilh, Gérard

doi:10.2174/187152008786847747

Cited by 27 publications

(25 citation statements)

References 90 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Because a recent study demonstrated the ability of igf-1 to induce vegfc and a Number of patients, unless otherwise specified. her2 = human epidermal growth factor receptor 2; igf-1 = insulinlike growth factor 1; igf-bp3 = insulin-like growth factor, binding protein 3; vegf-c = vascular endothelial growth factor C. therefore to promote lymphangiogenesis 15,16 , we explored the relations of serum igf-1 or igfbp3 with vegfc in breast cancer patients. The analysis revealed significant upregulation of serum igf-1, igfbp3, and vegfc in breast cancer patients compared with healthy control subjects.…”

Section: Discussionmentioning

confidence: 99%

“…apoptosis in many human cancer cell lines 19 -in particular, breast cancer cells 15 . However, the mechanisms by which igf-1 mediates cancer metastasis are poorly understood.…”

Section: Figure 1 Levels Of Insulin-like Growth Factor 1 (Igf-i) Igfmentioning

confidence: 99%

“…Increased expression of vegfc in primary tumours correlates with increased dissemination of tumour cells to regional lymph nodes in a variety of human carcinomas. In particular, increased vegfc expression has been closely related to lymphangiogenesis in breast cancer invasion and lymphatic metastasis 14 , and in a recent study, igf-1 was found to have the ability to induce and promote lymphangiogenesis 15 through induction of vegfc 16 .…”

Section: Introductionmentioning

confidence: 98%

See 2 more Smart Citations

Serum Insulin-Like Growth Factor 1 Correlates with the Risk of Nodal Metastasis in Endocrine-Positive Breast Cancer

et al. 2013

View full text Add to dashboard Cite

is activated after ligand binding of insulin, igf-1, or igf-2. Receptor stimulation leads to autophosphorylation of tyrosine residues and drives the activation of downstream signalling pathways, including the mapk (mitogen-activated protein kinase) and pi3k (phosphatidylinositol 3-kinase) cascades, which serve to influence key cell survival and proliferation pathways. The igfs are multifunctional peptides that regulate cell proliferation, differentiation, and apoptosis, which are important in tumourigenesis 3 .Unlike most other growth factors, igf peptides occur in large concentrations in the circulation and have systemic, hormonal, and local paracrine effects on cell behavior. In the circulation, igf-1 binds chiefly to the main igf binding protein, igfbp3. The literature on the relationship between breast cancer risk and circulating concentrations of igf-1 and igfbp3 had indicated an increased risk for women with increased levels of igf-1 and with low levels of igfbp3 6 .Increased igf signalling has been reported in clinical breast cancer specimens and has been linked to disease progression and recurrence 7-9 . Furthermore, overexpression of igf-1r has been found in most breast cancer cell lines, including endocrineresponsive MCF-7 human breast cancer cells 10,11 , which show active crosstalk between the estrogen receptor (er) and igf signalling 10,11 . In that light, estrogens appear to favour synergistic interactions with igfs, resulting in increased expression of igf-1r and growth. Conversely, igfs prime the activation of several kinases that are able to phosphorylate er and initiate gene expression mediated by the estrogen response element. Importantly, the anti-estrogen tamoxifen inhibits igf-1-mediated proliferation in er-positive breast cancer cells 12,13 .Lymph node metastasis is the hallmark of breast cancer progression; it is considered one of the most important prognostic factors. Recent studies have suggested that lymphangiogenesis plays an important ABSTRACTIncreased insulin-like growth factor (igf) signalling has been observed in breast cancer, including endocrine-responsive cancers, and has been linked to disease progression and recurrence. In particular, igf-1 has the ability to induce and promote lymphangiogenesis through the induction of vascular endothelial growth factor C (vegfc). In the present study, we analyzed serum and tumour samples from 60 patients with endocrine-positive breast cancer to determine the expression and the possible relationship of circulating igf-1, igf binding protein 3 (igfbp3), and vegfc with the presence of lymphatic metastasis and other immunohistochemical parameters. The analysis revealed a clear and significant correlation between high basal levels of igf-1, igfbp3, and vegfc and lymph node metastasis in endocrine-responsive breast cancer. In addition, expression of those molecules was significantly higher in breast cancer patients than in healthy control subjects. Those findings may enable more accurate prediction of prognosis in patients with breast cancer. KEY...

show abstract

Section: Discussionmentioning

confidence: 99%

“…apoptosis in many human cancer cell lines 19 -in particular, breast cancer cells 15 . However, the mechanisms by which igf-1 mediates cancer metastasis are poorly understood.…”

Section: Figure 1 Levels Of Insulin-like Growth Factor 1 (Igf-i) Igfmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 98%

See 1 more Smart Citation

Serum Insulin-Like Growth Factor 1 Correlates with the Risk of Nodal Metastasis in Endocrine-Positive Breast Cancer

et al. 2013

View full text Add to dashboard Cite

show abstract

“…HSP90 inhibitors may be an effective therapy to treat aromatase inhibitor-resistant breast cancers and improved efficacy can be achieved by combined use of a HSP90 inhibitor and an AKT inhibitor [279].…”

Section: Targeting Crosstalk Of Estrogen Receptor With Combination Ofmentioning

confidence: 99%

RETRACTED ARTICLE: Regulation of estrogen receptor signaling in breast carcinogenesis and breast cancer therapy

Zhou

Qiao

Shetty

et al. 2013

Cell. Mol. Life Sci.

View full text Add to dashboard Cite

Estrogen and estrogen receptors (ERs) are critical regulators of breast epithelial cell proliferation, differentiation, and apoptosis. Compromised signaling vis-à-vis the estrogen receptor is believed © Springer Basel 2013 yow4@pitt.edu. ), which predicts for response to endocrine-based therapy; however, innate or acquired resistance to endocrinebased drugs remains a serious challenge. The complexity of regulation for estrogen signaling coupled with the crosstalk of other oncogenic signaling pathways is a reason for endocrine therapy resistance. Alternative strategies that target novel molecular mechanisms are necessary to overcome this current and urgent gap in therapy. A thorough analysis of estrogen-signaling regulation is critical. In this review article, we will summarize current insights into the regulation of estrogen signaling as related to breast carcinogenesis and breast cancer therapy. NIH Public Access

show abstract

“…Tumor growth can be determined by the speed with which tumor cells progress towards death and elimination, in addition to the progression of malignant cells (Mester and Redeuilh, 2008). Therefore, the inhibition of tumor growth and induction of tumor cell death are elective therapeutic strategies for the control of tumor progression (Yang et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

O-naphthoquinone isolated from Capraria biflora L. induces selective cytotoxicity in tumor cell lines

et al. 2015

View full text Add to dashboard Cite

ABSTRACT.Biflorin is an o-naphthoquinone isolated from the roots of the plant Capraria biflora L. (Scrophulariaceae). In this study, the cytotoxic effects of biflorin were verified, and late apoptosis was detected in various cancer cell lines by in situ analysis. The cytotoxicity was further evaluated exclusively for 48 h of treatment in different tumor and non-tumor cell lines (Hep-2, HeLa, HT-29, A-375, and A-549, and HEK-293, respectively). The results indicated that biflorin induced selective cytotoxicity in tumor cells. HeLa cells were more susceptible to biflorin, followed by HT-29, A-549, A-375, and Hep-2 at all concentrations (range 5-50 µg/mL), and the highest half-maximal inhibitory concentration IC 50 (56.01 ± 1.17 µg/mL) was observed in HEK-293 cells. Late apoptotic/necrotic events, observed by in situ immunostaining with Annexin V, varied with each cell line; an increase in late apoptotic events was observed corresponding to the increase in biflorin dosage. Hep-2 cells showed a greater percentage of late apoptotic events among the tumor cell lines when treated with higher concentrations of biflorin (69.63 ± 2.28%). The non-tumor HEK-293 line showed greater resistance to late apoptotic events, as well as a lower level of cytotoxicity (77.69 ± 6.68%) than the tested tumor lines. The data presented indicate that biflorin showed an important, possibly selective, cytotoxicity against tumor cell lines, thereby revealing a promising novel substance with potential anticancer activity for tumor therapy.

show abstract

Proliferation of Breast Cancer Cells: Regulation, Mediators, Targets for Therapy

Cited by 27 publications

References 90 publications

Serum Insulin-Like Growth Factor 1 Correlates with the Risk of Nodal Metastasis in Endocrine-Positive Breast Cancer

Serum Insulin-Like Growth Factor 1 Correlates with the Risk of Nodal Metastasis in Endocrine-Positive Breast Cancer

RETRACTED ARTICLE: Regulation of estrogen receptor signaling in breast carcinogenesis and breast cancer therapy

O-naphthoquinone isolated from Capraria biflora L. induces selective cytotoxicity in tumor cell lines

Contact Info

Product

Resources

About