Identification of Insulin and Insulin-like Growth Factor I (IGF I) Receptors in Ovarian Cancer Tissue

Beck, Eberhard; Russo, P.; Gliozzo, Biancamaria; Jaeger, Wolfram; Papa, Vincenzo; Wildt, L.; Pezzino, V.; Lang, N.

doi:10.1006/gyno.1994.1115

Cited by 43 publications

(22 citation statements)

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“…16 18) It has been shown that IGFR is expressed in normal OSE cells and ovarian carcinoma specimens. 18,[22][23][24] Also, in vitro studies have shown that IGF1 and IGFR mediate adherent proliferation of the human ovarian carcinoma cell lines OVCAR-3 and CaOV-3. 22) These findings suggest that the LH/CG-LH/CGR and IGF1-IGFR systems are involved in growth of normal and neoplastic OSE cells.…”

Section: Discussionmentioning

confidence: 99%

Roles of luteinizing hormone/chorionic gonadotropin receptor in anchorage‐dependent and ‐independent growth in human ovarian surface epithelial cell lines

et al. 2003

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Epithelial ovarian carcinomas are thought to arise from cells of ovarian surface epithelium (OSE) covering the free surface of the human ovary. Two immortalized human cell lines, OSE2a (non-tumorigenic) and OSE2b-2 (tumorigenic), were previously established from normal OSE cells of a reproductive-age patient. In the present study, we found that expression of luteinizing hormone (LH)/chorionic gonadotropin (CG) receptor (LH/CGR) is present in OSE2a cells and absent in OSE2b-2 cells. In OSE2a cells, a low concentration (10 3 mIU/ml) of CG enhanced anchorage-dependent growth via up-regulation of insulin-like growth factor-1 (IGF1), whereas a high concentration (10 5 mIU/ml) of CG induced anchorage-independent growth and down-regulation of IGF1 expression. To investigate involvement of other genes in LH/CGRrelated tumorigenicity, we compared cDNA expression arrays of OSE2a and OSE2b-2 cells, and found that the following genes had lower expression in OSE2b-2 than in OSE2a: integrin β β β β1, intercellular adhesion molecule-1 (ICAM1), and Waf1/Cip1. Subsequent semiquantitative reverse transcription polymerase chain reaction using OSE2a cells showed that expression of integrin β β β β1 pithelial ovarian carcinoma constitutes approximately 90% of ovarian malignancies, and is generally thought to derive from ovarian surface epithelium (OSE), 1) which descends from embryonic coelomic mesothelium and gives rise to the mülle-rian ducts.2) A number of gene alterations related to ovarian carcinogenesis have been found in studies using ovarian carcinoma specimens and cell lines. There have been reports of inactivation of tumor suppressor genes (p53, BRCA1, BRCA2 and PTEN) and activation of oncogenes (Ki-ras, c-erbB-2, c-myc, AKT2 and PIK3CA) in cases of epithelial ovarian carcinoma.3)

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Section: Discussionmentioning

confidence: 99%

Roles of luteinizing hormone/chorionic gonadotropin receptor in anchorage‐dependent and ‐independent growth in human ovarian surface epithelial cell lines

et al. 2003

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“…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%

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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“…A possible link between the insulin-like growth factor (IGF) system and ovarian cancer stems from the findings that IGF-I levels were found to be significantly higher in cyst fluid from invasive malignant epithelial ovarian neoplasms compared to cyst fluid from benign neoplasms [5], and that IGF-I and related binding proteins (IGFBP) are expressed in epithelial ovarian cancer cells [6, 7]. IGFBPs act as regulators of IGF-I action, and IGFBP-3 was found to be lower in ovarian cancer patients compared to controls [8].…”

Section: Introductionmentioning

confidence: 99%

Association between Components of the Insulin-Like Growth Factor System and Epithelial Ovarian Cancer Risk

Maso¹,

Augustin²,

Franceschi³

et al. 2004

Oncology

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Background: Components of the insulin-like growth factor (IGF) system have been associated with several cancers, but very few studies are available for ovarian cancer. Methods: A case-control study conducted between 1999 and 2003 in Italy, including a total of 59 women with incident, histologically confirmed ovarian cancer and 108 controls admitted to the same hospital network as cases, for acute non-neoplastic diseases. All subjects were interviewed using a validated questionnaire. Results: After adjustment for potential confounders, the multivariate odds ratios for the highest versus the lowest tertile of various IGF components were 0.6 (95% confidence interval, CI: 0.2–1.4) for free IGF-I, 0.4 (CI: 0.1–1.5) for total IGF-I, 2.6 (CI: 0.9–6.9) for IGF-binding protein (IGFBP)-1, and 0.2 (CI: 0.0–0.6) for IGFBP-3. Conclusions: This study suggests a protective role of IGFBP-3 and a positive association of IGFBP-1 with ovarian cancer. The complex role of the IGF system in ovarian carcinogenesis deserves further clarification.

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Identification of Insulin and Insulin-like Growth Factor I (IGF I) Receptors in Ovarian Cancer Tissue

Cited by 43 publications

References 0 publications

Roles of luteinizing hormone/chorionic gonadotropin receptor in anchorage‐dependent and ‐independent growth in human ovarian surface epithelial cell lines

Roles of luteinizing hormone/chorionic gonadotropin receptor in anchorage‐dependent and ‐independent growth in human ovarian surface epithelial cell lines

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

Association between Components of the Insulin-Like Growth Factor System and Epithelial Ovarian Cancer Risk

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