Growth factors and ovarian cancer

Langdon, Simon P.; Smyth, J. F.

doi:10.1677/erc.0.0050283

Cited by 6 publications

(7 citation statements)

References 72 publications

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“…In particular, (1) fibroblast growth factors 6 and 7 (FGF-6 and -7), which are mitogenic; 45 (2) neurotrophin-4 (NT-4), which is a cell survival factor; 46 (3) placental growth factor (PIGF), which is angiogenic and works with VEGF to promote pathological new blood vessel growth; 47 and (4) Parc, which anchors p53 in the cytoplasm 48 and is therefore antiapoptotic, were downregulated by anti-IGFBP-2 antibody. These findings may therefore have important clinical implications in the management of ovarian cancer.…”

Section: Discussionmentioning

confidence: 99%

“…The growth and progression of this disease is driven by a variety of regulators including growth factors, hormones and cytokines. 2 Insulin-like growth factors (IGFs) and their binding proteins (BPs) have important roles in the normal ovary and exert intraovarian control in the replication and differentiation process of folliculogenesis; 3,4 they have also been identified in a number of ovarian tumors [5][6][7][8][9] and in ovarian cancer cell line models. [10][11][12][13][14] Recent studies have specifically demonstrated that IGFBP-2 levels are dramatically high in the sera of women with epithelial ovarian cancer, with elevation being positively correlated with the aggressiveness of the tumor and expression of the tumor marker CA125.…”

Section: Introductionmentioning

confidence: 99%

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Insulin-like growth factor binding protein-2 stimulates proliferation and activates multiple cascades of the mitogen-activated protein kinase pathways in NIH-OVCAR3 human epithelial ovarian cancer cells

Chakrabarty

Kondratick²

2006

Cancer Biology & Therapy

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Insulin-like growth factor binding protein-2 (IGFBP-2), the second most abundant IGFBP in the circulation, is dramatically increased in the serum and ovarian cyst fluid of women with epithelial ovarian cancer. The specific role of IGFBP-2 in ovarian carcinogenesis remains elusive. Using NIH-OVCAR3 human epithelial ovarian cancer cells, we have evaluated the effects of IGFBP-2 and its antibody on cell proliferation, activation of mitogenactivated protein kinase (MAP kinase) pathways and on cytokine expression. Treatment of the cells with IGFBP-2 stimulates cell growth significantly (p < .05) and potentiates the activation of (1) the extracellular signal regulated kinase (ERK1/2) signaling pathway, which transduces cell-specific growth and differentiation signals; (2) the stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK) pathway, which is activated by environmental stresses, inflammatory cytokines, growth factors and G-protein coupled receptor (GPCR) agonists; and (3) the p38 MAP kinase pathway, which mediates inflammatory and stress responses. Suppression of IGFBP-2, with its neutralizing antibody, significantly (p < .05) retards cell growth, blocks the activation of all three cascades of the MAPK pathways and downregulates the expression of a number of potential cancerpromoting cytokines. These novel findings may have important clinical implications for developing innovative strategies for the treatment and management of ovarian cancer.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Insulin-like growth factor binding protein-2 stimulates proliferation and activates multiple cascades of the mitogen-activated protein kinase pathways in NIH-OVCAR3 human epithelial ovarian cancer cells

Chakrabarty

Kondratick²

2006

Cancer Biology & Therapy

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“…In malignant ovarian tumors, PDGF is overexpressed and has been dosed in a large number of samples, together with its receptors, which are present in malignant ascites too [ 6 ]. Moreover, patients with ovarian cancer expressing the PDGF receptor demonstrate an overall shorter survival time compared with those whose tumors did not express the receptor [ 9 ]. PDGFA and -B have been found in serum of patients with advanced International Federation of Gynecology and Obstetrics stages (III–IV).…”

Section: Main Pro-angiogenic Factorsmentioning

confidence: 99%

Biological Pathways Involved in Tumor Angiogenesis and Bevacizumab Based Anti-Angiogenic Therapy with Special References to Ovarian Cancer

Loizzi

Vecchio

Gargano

et al. 2017

IJMS

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The creation of new blood vessels from existing ones, which is a mechanism called “angiogenesis”, is essential in cancer to supply cancerous growth. Moreover, the development and the progression of the tumor and its metastases are the result of an efficient vascular response. Cancer cells release and activate different angiogenic growth factors and their receptors in the tumor microenvironment to promote the angiogenic process. The most important pro-angiogenic factor is the “Vascular Endothelial Growth Factor” (VEGF) because of its mitogen activity on vascular endothelium. Bevacizumab is a monoclonal antibody that obstructs the binding of circulating vascular endothelial growth factor to its receptors and has been approved for the treatment of primary and recurrent ovarian cancer but also for many other solid tumors.

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“…Often the diagnosis of ovarian cancer occurs late and the treatment options are limited [1]. Epithelial ovarian cancer arises primarily from neoplastic transformation of the ovarian surface epithelium (OSE), a layer of flat or cuboidal cells that cover the surface of the ovary [2, 3]. Some high grade serous ovarian cancers may also arise from fallopian tubal epithelia [2].…”

Section: Introductionmentioning

confidence: 99%

“…Some high grade serous ovarian cancers may also arise from fallopian tubal epithelia [2]. Hormones, growth factors and cytokine-dependent activation of cellular signaling pathways are critical for the regulation of OSE proliferation, and a thorough understanding of these signaling pathways is necessary to achieve earlier detection and develop novel therapies [3, 4]. …”

Section: Introductionmentioning

confidence: 99%

Mixed lineage kinase 3 is required for matrix metalloproteinase expression and invasion in ovarian cancer cells

Zhan

Saab

Modi

et al. 2012

Experimental Cell Research

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Mixed lineage kinase 3 (MLK3) is a mitogen-activated protein kinase kinase kinase (MAP3K) that activates MAPK signaling pathways and regulates cellular responses such as proliferation, migration and apoptosis. Here we report high levels of total and phospho-MLK3 in ovarian cancer cell lines in comparison to immortalized nontumorigenic ovarian epithelial cell lines. Using small interfering RNA (siRNA)-mediated gene silencing, we determined that MLK3 is required for the invasion of SKOV3 and HEY1B ovarian cancer cells. Furthermore, mlk3 silencing substantially reduced matrix metalloproteinase (MMP) -1, -2, -9 and -12 gene expression and MMP-2 and -9 activities in SKOV3 and HEY1B ovarian cancer cells. MMP-1, -2, -9 and-12 expression, and MLK3-induced activation of MMP-2 and MMP-9 requires both extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase activities. In addition, inhibition of activator protein-1 (AP-1) reduced MMP-1, MMP-9 and MMP-12 gene expression. Collectively, these findings establish MLK3 as an important regulator of MMP expression and invasion in ovarian cancer cells.

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Growth factors and ovarian cancer

Cited by 6 publications

References 72 publications

Insulin-like growth factor binding protein-2 stimulates proliferation and activates multiple cascades of the mitogen-activated protein kinase pathways in NIH-OVCAR3 human epithelial ovarian cancer cells

Insulin-like growth factor binding protein-2 stimulates proliferation and activates multiple cascades of the mitogen-activated protein kinase pathways in NIH-OVCAR3 human epithelial ovarian cancer cells

Biological Pathways Involved in Tumor Angiogenesis and Bevacizumab Based Anti-Angiogenic Therapy with Special References to Ovarian Cancer

Mixed lineage kinase 3 is required for matrix metalloproteinase expression and invasion in ovarian cancer cells

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