Growth inhibition and differentiation of the human colon carcinoma cell line, Caco‐2, by constitutive expression of insulin‐like growth factor binding protein‐3

MacDonald, Richard G.; Schaffer, Beverly S.; Kang, Il Jun; Hong, Sungjun; Kim, Eun J.; Park, Jung H.Y.

doi:10.1046/j.1440-1746.1999.01803.x

Cited by 19 publications

(6 citation statements)

References 41 publications

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“…The involvement of IGFBP-3 in the inhibition of cell growth is evident when human IGFBP-3 cDNA is transfected into mammalian cell lines like colon cancer cells (MacDonald et al, 1999), human breast cells (Firth et al, 1998a) and mouse fibroblast cells (Cohen et al, 1993). Apoptosis inducing effect of IGFBP-3 has been demonstrated to be an IGF-dependent as well as an IGF-independent process.…”

Section: Igf-independent Role Of Igfbp-3 In Apoptosismentioning

confidence: 99%

Insulin-Like Growth Factor Binding Protein-3 (IGFBP-3): Unraveling the Role in Mediating IGF-Independent Effects Within the Cell

Shrivastav

Bhardwaj

Pathak

et al. 2020

Front. Cell Dev. Biol.

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Section: Igf-independent Role Of Igfbp-3 In Apoptosismentioning

confidence: 99%

Insulin-Like Growth Factor Binding Protein-3 (IGFBP-3): Unraveling the Role in Mediating IGF-Independent Effects Within the Cell

Shrivastav

Bhardwaj

Pathak

et al. 2020

Front. Cell Dev. Biol.

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“…More IGF can become bioavailable to stimulate the IGF-1R due to diminished IGFBP sequestration; this may be achieved by either reduced IGFBP production and/or by increased IGFBP proteolysis. For example, when Caco-2 human colon carcinoma cells were stably transfected with an IGFBP-3 cDNA expression construct, they achieved a much lower final cell density after one-and-a-half weeks of growth and began transcription of sucrase-isomaltase, a marker of enterocyte differentiation; in Caco-2 cells transfected with empty plasmid, IGFBP-3 was undetectable, growth was unimpaired, and sucrase-isomaltase was not produced (MacDonald et al, 1999). Increased proteolysis of IGFBP-3 has been shown in prostate cancer by PSA (Cohen et al, 1992), cathepsin D (Nunn et al, 1997), urokinase and plasminogen-activator (Angelloz-Nicoud and Binoux, 1995).…”

Section: Igfs and Igfbps In Carcinogenesismentioning

confidence: 99%

Role of insulin-like growth factors and their binding proteins in growth control and carcinogenesis

Grimberg

Cohen²

2000

J. Cell. Physiol.

450

281

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Interest in the role of the insulin-like growth factor (IGF) axis in growth control and carcinogenesis has recently been increased by the finding of elevated serum insulin-like growth factor I (IGF-I) levels in association with three of the most prevalent cancers in the United States: prostate cancer, colorectal cancer, and lung cancer. IGFs serve as endocrine, autocrine, and paracrine stimulators of mitogenesis, survival, and cellular transformation. These actions are mediated through the type 1 IGF-receptor (IGF-1R), a tyrosine kinase that resembles the insulin receptor. The availability of free IGF for interaction with the IGF-1R is modulated by the insulin-like growth factor-binding proteins (IGFBPs). IGFBPs, especially IGFBP-3, also have IGF-independent effects on cell growth. IGF-independent growth inhibition by IGFBP-3 is believed to occur through IGFBP-3-specific cell surface association proteins or receptors and involves nuclear translocation. IGFBP-3-mediated apoptosis is controlled by numerous cell cycle regulators in both normal and disease processes. IGFBP activity is also regulated by IGFBP proteases, which affect the relative affinities of IGFBPs, IGFs and IGF-1R. Perturbations in each level of the IGF axis have been implicated in cancer formation and progression in various cell types.

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“…Macdonald et al (90) in 1999 demonstrated that the human colon carcinoma cell line, Caco-2, which was stably transfected with an IGFBP-3 expression construct, grew more slowly in vitro than the cells transfected with a control vector.…”

Section: Igf-ii Expressionmentioning

confidence: 99%

The Effects of Insulin-Like Growth Factors on Tumorigenesis and Neoplastic Growth

2000

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Several decades of basic and clinical research have demonstrated that there is an association between the insulin-like growth factors (IGFs) and neoplasia. We begin with a brief discussion of the function and regulation of expression of the IGFs, their receptors and the IGF-binding proteins (IGFBPs). A number of investigational interventional strategies targeting the GH or IGFs are then reviewed. Finally, we have assembled the available scientific knowledge about this relationship for each of the major tumor types. The tumors have been grouped together by organ system and for each of the major tumors, various key elements of the relationship between IGFs and tumor growth are discussed. Specifically these include the presence or absence of autocrine IGF-I and IGF-II production; presence or absence of IGF-I and IGF-II receptor expression; the expression and functions of the IGFBPs; in vitro and in vivo experiments involving therapeutic interventions; and available results from clinical trials evaluating the effect of GH/IGF axis down-regulation in various malignancies. (Endocrine Reviews 21: 2000)

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Growth inhibition and differentiation of the human colon carcinoma cell line, Caco‐2, by constitutive expression of insulin‐like growth factor binding protein‐3

Cited by 19 publications

References 41 publications

Insulin-Like Growth Factor Binding Protein-3 (IGFBP-3): Unraveling the Role in Mediating IGF-Independent Effects Within the Cell

Insulin-Like Growth Factor Binding Protein-3 (IGFBP-3): Unraveling the Role in Mediating IGF-Independent Effects Within the Cell

Role of insulin-like growth factors and their binding proteins in growth control and carcinogenesis

The Effects of Insulin-Like Growth Factors on Tumorigenesis and Neoplastic Growth

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