Molecular cloning of IGFBP-5 from SCLC cell lines and expression of IGFBP-4, IGFBP-5 and IGFBP-6 in lung cancer cell lines and primary tumours

Wegmann, Barbara; Schöneberger, Hans J; Kiefer, Paul; Jaques, Gabriele; Brandscheid, Detlef; Havemann, K.

doi:10.1016/0959-8049(93)90298-t

Cited by 20 publications

(10 citation statements)

References 27 publications

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“…IGFBP‐4 protein expression was significantly lower in primary renal cancer tissues; however, the expression was high in metastatic renal cancer tissues. Although this result has not been reported previously in other cancers, IGFBP‐4 is expressed in lung and gastric cancer 17, 18. In contrast, IGFBP‐4 has been reported to inhibit tumor and colony formation in prostate and colon cancer 19–21.…”

Section: Discussioncontrasting

confidence: 74%

IGFBP‐4 activates the Wnt/beta‐catenin signaling pathway and induces M‐CAM expression in human renal cell carcinoma

Ueno

Hirata

Majid

et al. 2011

Intl Journal of Cancer

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The Wnt/b-catenin signaling pathway is inactivated by Wnt antagonists in most cancers and IGFBP-4 is an antagonist of the Wnt/ b-catenin signaling pathway. However, the function of IGFBP-4 is not currently understood in renal cell carcinoma (RCC). We initially found that the expression of IGFBP-4 was significantly lower in primary RCC and higher in metastatic RCC compared to normal human kidney tissues. To assess the function of IGFBP4, we established IGFBP4 transfectants (primary renal cancer cell line) and performed functional analyses including Tcf reporter assays, cell viability, invasive capability, mortality, and in vivo tumor growth. Interestingly IGFBP-4 transfectants promoted cell growth (in vitro and in vivo), invasion, and motility in primary renal cancer. Tcf transcriptional activity was significantly increased in IGFBP-4 transfectants compared to mock cells and b-catenin expression was increased. Also the b-catenin downstream effector, MT1-MMP showed increased expression in IGFBP4 transfectants. Additionally IGFBP4 induced the expression of M-CAM, a marker of tumor progression. In order to assess the role of IGFBP4 in metastatic renal cancer, IGFBP-4 mRNA in a metastatic renal cancer cell lines (ACHN) was knocked-down using a siRNA technique. The cell growth and motility was decreased in si-IGFBP4 transfected ACHN cells compared to cells transfected with control siRNA. Tcf activity in ACHN cells was also decreased with si-IGFBP-4 transfection. This is a first report documenting that IGFBP-4 expression in RCC activates cell growth, metastasis, Wnt/beta-catenin signaling and may be involved in RCC metastasis.

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Section: Discussioncontrasting

confidence: 74%

IGFBP‐4 activates the Wnt/beta‐catenin signaling pathway and induces M‐CAM expression in human renal cell carcinoma

Ueno

Hirata

Majid

et al. 2011

Intl Journal of Cancer

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“…Dysregulation at several levels of the axis occur in human cancer (LeRoith et al 1995). This axis has been characterized in many human cancer models, including breast (Sachdev & Yee 2001), hepatocellular (Hanafusa et al 2002, lung (Wegmann et al 1993), colon (Giovannucci 2001), ovary (Krywicki et al 1993), testes (Drescher et al 1997), leukemia (Wex et al 1998), adrenal (Boulle et al 2001), brain (Zumkeller & Westphal 2001) and prostate (Djavan et al 2001).…”

Section: Igfbp-3 -A Biological Mediator Of Cancer Cell Apoptosismentioning

confidence: 99%

Nuclear effects: unexpected intracellular actions of insulin-like growth factor binding protein-3

Cohen²

2002

Journal of Endocrinology

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Insulin-like growth factor (IGF) binding protein (IGFBP)-3 has been shown to be a growth inhibitory, apoptosis-inducing molecule by virtue of its ability to bind IGFs, in addition to previously demonstrated IGFindependent effects. The recent discovery of the interaction between nuclear IGFBP-3 and 9-cis retinoic acid receptor-(retinoid X receptor RXR ), a nuclear receptor, and its involvement in the regulation of transcriptional signaling and apoptosis represents an important paradigm shift in the understanding of IGFBP function. RXR is required for the apoptosis-inducing effects of IGFBP-3. IGFBP-3 and RXR ligands are additive in inducing apoptosis in cancer cells. IGFBP-3 has direct effects on gene transcription, as RXR response element reporter signaling was enhanced and the all-trans retinoic acid receptor response element reporter signaling was inhibited. Accumulating evidence further confirms IGF-independent functions of this multifunction binding protein. Other binding proteins, in addition to other members of the IGF axis, have now been described in the nucleus and are postulated to have effects on transcriptional events. Investigation into these new interactions will expose new protein partners in the interface between the nuclear receptor and growth factor pathways and reveal new targets to be exploited in the treatment of cancer and other diseases.

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“…1F). There are six unique IGF-binding proteins, which appear to have tumor-specific patterns of expression , Cohen et al 1993, Guo et al 1993, Wegmann et al 1993, Bernardini et al 1994, Vincent et al 1994. Functionally, the end result of altering IGF-binding protein levels upon IGF-II activity depends upon individual binding proteins.…”

Section: Igf-ii Overexpressionmentioning

confidence: 99%

Involvement of IGF-II in human cancer

Toretsky

Helman²

1996

Journal of Endocrinology

137

102

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IGF-II is a regulatory peptide which appears to be involved significantly in the progression of many tumors, while minimally involved in post-fetal non-tumor tissue. Interruption of IGF-II pathways therefore offers the possibility of tumor control with a high therapeutic index. Investigators should continue to evaluate tumors for the involvement of IGF-II as well as investigate clinically relevant means of disrupting those pathways.

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Molecular cloning of IGFBP-5 from SCLC cell lines and expression of IGFBP-4, IGFBP-5 and IGFBP-6 in lung cancer cell lines and primary tumours

Cited by 20 publications

References 27 publications

IGFBP‐4 activates the Wnt/beta‐catenin signaling pathway and induces M‐CAM expression in human renal cell carcinoma

IGFBP‐4 activates the Wnt/beta‐catenin signaling pathway and induces M‐CAM expression in human renal cell carcinoma

Nuclear effects: unexpected intracellular actions of insulin-like growth factor binding protein-3

Involvement of IGF-II in human cancer

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