Human osteosarcoma (U‐2 OS) cells express both insulin‐like growth factor‐I (IGF‐I) receptors and insulin‐like growth factor‐II/mannose‐6‐phosphate (IGF‐II/M6P) receptors and synthesize IGF‐II: Autocrine growth stimulation by IGF‐II via the IGF‐I receptor

Raile, Klemens; Höflich, Andreas; Kessler, Ulrike; Yang, Yi; Pfuender, M; Blum, Werner; Kolb, Helmut J.; Schwarz, Hans; Kieß, Wieland

doi:10.1002/jcp.1041590317

Cited by 68 publications

(46 citation statements)

References 43 publications

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“…The ROS 17/2.8 and U-2 cultures treated with dexamethasone contained nodules that stained with antibodies to proteins unique to cartilage and bone (Table 1). This is consistent with studies showing osteosarcoma cells form bone in vivo [23,33,43]. Phenotypic markers characteristic for smooth muscle and endothelial cells also were seen with dexamethasone treatment.…”

Section: Discussionsupporting

confidence: 91%

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Osteosarcoma Cells Differentiate into Phenotypes from all Three Dermal Layers

Russinoff

Miran

Gowda

et al. 2011

Clinical Orthopaedics &Amp; Related Research

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Section: Discussionsupporting

confidence: 91%

“…U-2 cells were obtained from ATCC (Manassas, VA, USA). This line originated from a moderately differentiated sarcoma of the tibia of a 15-year-old girl [13,14,43]. Both osteosarcoma cell lines have an extended proliferation potential.…”

Section: Methodsmentioning

confidence: 99%

Osteosarcoma Cells Differentiate into Phenotypes from all Three Dermal Layers

Russinoff

Miran

Gowda

et al. 2011

Clinical Orthopaedics &Amp; Related Research

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“…In different human osteosarcoma cell lines an inhibition of the IGF-1-and -2-stimulated uptake of thymidine as well as a partial inhibition of the basal DNA synthesis was observed when the IGF-1R was blocked by monoclonal antibody a-IR3 (Raile et al, 1994). Thus, raising the neutralisation capacities for IGF-2 in the space of Disse as well as blocking the IGF-1R may be interesting strategies to prevent the formation of HCC in patients at risk of developing this malignancy.…”

Section: Discussionmentioning

confidence: 99%

Focal overexpression of insulin-like growth factor 2 by hepatocytes and cholangiocytes in viral liver cirrhosis

et al. 2003

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Insulin-like growth factor (IGF)-2 is overexpressed in hepatocellular carcinoma and accompanying dysplastic lesions. IGF-2 signalling is mediated through IGF-1 receptor (IGF-1R), while mannose 6-phosphate/insulin-like growth factor-2 receptor (M6P/IGF-2R) controls pericellular levels of free IGF-2. We studied, by in situ hybridisation and immunohistology, 18 liver specimens with cirrhosis of different aetiology without neoplastic or dysplastic lesions. Immunohistology was also performed for insulin receptor IGF-1R and IGF-binding proteins 3 and 4. High focal levels of IGF-2 RNA were found in some hepatocytes of all livers with HBV-or HCV-induced cirrhosis (n ¼ 10), but in only one of the cirrhoses with nonviral aetiology (n ¼ 8). IGF-2 was overexpressed in biliary duct epithelial cells in one case. Compared with noncirrhotic liver, all cirrhotic specimens showed reduced hepatocellular expression of M6P/IGF-2R protein, which contrasted with enhanced expression in perisinusoidal cells. Immunostaining for the other antigens did not reveal significant differences. Upregulation of IGF-2 in some hepatocytes may lead to high focal IGF-2 levels sufficient to saturate local IGF-2 binding capacities, and may result in an increased susceptibility to cellular dedifferentiation and, ultimately, liver cancer. Downregulation of hepatocellular M6P/IGF-2R and upregulation of IGF-2 seem to be early events in hepatocarcinogenesis prior to the appearance of morphologically distinct dysplastic lesions. Elevated focal IGF-2 transcript levels may therefore indicate an increased risk for hepatocellular and cholangiocellular carcinomas.

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“…Immunoactive IGF-II and mRNA for IGF-II were found in U-2 OS human osteosarcoma cells. 30 mRNA for IGF-I and IGF-II and receptors for IGF-I and IGF-II were demonstrated in surgical specimens obtained from patients with osteosarcomas. 31 Thus, therapeutic agents that suppress the synthesis of tumoral IGF-II may be useful for the treatment of patients with malignancies, including patients with osteosarcomas that require IGF-II as an autocrine growth factor.…”

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confidence: 97%

Inhibition of proliferation in human MNNG/HOS osteosarcoma and SK‐ES‐1 Ewing sarcoma cell lines in vitro and in vivo by antagonists of growth hormone‐releasing hormone

Braczkowski

Schally

Płonowski

et al. 2002

Cancer

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BACKGROUNDAntagonists of growth hormone‐releasing hormone (GH‐RH) can inhibit the proliferation of various tumors either indirectly through the suppression of the pituitary growth hormone/hepatic insulin‐like growth factor I (IGF‐I) axis and the lowering of serum IGF‐I concentration or directly by reducing the levels of IGF‐I and IGF‐II and their mRNA expression in tumors and blocking the effect of autocrine GH‐RH. In this study, the authors investigated the effects of the GH‐RH antagonist JV‐1‐38 on MNNG/HOS human osteosarcoma and SK‐ES‐1 human Ewing sarcoma cell lines.METHODSMale nude mice bearing subcutaneous xenografts of MNNG/HOS or SK‐ES‐1 tumors were treated subcutaneously with JV‐1‐38 at a dose of 20 μg twice daily for 4 weeks. The concentrations of IGF‐I and IGF‐II in serum and in tumor tissue were measured by radioimmunoassay. Tumor and liver levels of mRNA for IGF‐I and IGF‐II were determined by reverse transcriptase‐polymerase chain reaction analysis. The effects of JV‐1‐38, IGF‐I, and IGF‐II on cell proliferation in vitro were evaluated.RESULTSGH‐RH antagonist significantly (P < 0.05) inhibited the tumor volume and tumor weight of MNNG/HOS and SK‐ES‐1 tumors by > 50% after 4 weeks and increased tumor doubling time. JV‐1‐38 lowered the serum IGF‐I level, decreased the expression of mRNA for IGF‐I in the liver, and significantly (P < 0.05–0.01) reduced the concentration of IGF‐II and mRNA levels for IGF‐II in both sarcomas. The concentration of IGF‐I was lowered only in SK‐ES‐1 tumors. In vitro, the proliferation of SK‐ES‐1 and MNNG/HOS cells was inhibited by JV‐1‐38 and by antisera to IGF‐I and IGF‐II.CONCLUSIONSThe inhibition of MNNG/HOS osteosarcoma and SK‐ES‐1 Ewing sarcoma by GH‐RH antagonists was linked to a suppression of IGF‐II production in tumors. However, in SK‐ES‐1 tumors, the effects on IGF‐I also may be involved. Cancer 2002;95:1735–45. © 2002 American Cancer Society.DOI 10.1002/cncr.10865

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Human osteosarcoma (U‐2 OS) cells express both insulin‐like growth factor‐I (IGF‐I) receptors and insulin‐like growth factor‐II/mannose‐6‐phosphate (IGF‐II/M6P) receptors and synthesize IGF‐II: Autocrine growth stimulation by IGF‐II via the IGF‐I receptor

Abstract: 1) U-2 OS cells express IGF-I and IGF-II/M6P receptors. 2) U-2 OS tumor cells respond to the addition of exogenous IGF-I and IGF-II with an increase of DNA synthesis.(ABSTRACT TRUNCATED AT 400 WORDS)

Cited by 68 publications

References 43 publications

Osteosarcoma Cells Differentiate into Phenotypes from all Three Dermal Layers

Osteosarcoma Cells Differentiate into Phenotypes from all Three Dermal Layers

Focal overexpression of insulin-like growth factor 2 by hepatocytes and cholangiocytes in viral liver cirrhosis

Inhibition of proliferation in human MNNG/HOS osteosarcoma and SK‐ES‐1 Ewing sarcoma cell lines in vitro and in vivo by antagonists of growth hormone‐releasing hormone

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