Biochemical and Biophysical Research Communications
Regular ArticleInsulin-like Growth Factor Binding Protein-3 Induces Apoptosis in MCF7 Breast Cancer Cells
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Loss of the aryl hydrocarbon receptor increases tumorigenesis in p53-deficient mice
2022, Toxicology and Applied PharmacologyCitation Excerpt :Both AhR and p53 directly induce the transcription of the cyclin-dependent kinase inhibitor 1A (CDKN1A, p21, CIP1, WAF1), initiating growth arrest (O'Donnell et al., 2017; El-Deiry et al., 1993). Both proapoptotic Bcl-2-associated X protein (BAX) and insulin-like growth factor binding protein-3 (IGFBP3) are also transcriptionally regulated by p53 and AhR (Miyashita and Reed, 1995; Buckbinder et al., 1995; Matikainen et al., 2001; Nickerson et al., 1997). Phosphatase and tensin homolog (PTEN) inhibits cell transformation, invasion, and migration, and is regulated indirectly by AhR and directly by p53 (Stambolic et al., 2001; Chang et al., 2014).
Roles and molecular mechanisms of physical exercise in cancer prevention and treatment
2021, Journal of Sport and Health ScienceCitation Excerpt :Some studies involving postmenopausal women have shown that after 6 months of walking training, IGF-1 and IGF-3 are significantly lower in exercising women than in non-exercising women.67 IGF binding protein-3 (IGFBP-3) regulates the mitosis of IGF, and its anti-apoptosis effect is inhibited in breast cancer cells.68 Studies have shown that weight loss reduces levels of IGF-1, insulin, and leptin in mouse models of skin cancer, leading to the reduction of IGF-1-related signaling pathways, including rat sarcoma-mitogen-activated protein kinase (Ras-MAPK) proliferation and protein kinase B (known as Akt) -phosphatidylinositol 3 kinase (PKB/AKt-PI3K) anti-apoptosis; IGF-1 targets PKB/Akt and the adenosine monophosphate(AMP)-activated protein kinase pathway, leading to cell cycle inactivation and cancer suppression.69
Injectable hyaluronic acid down-regulates interferon signaling molecules, IGFBP3 and IFIT3 in the bovine intervertebral disc
2017, Acta BiomaterialiaCitation Excerpt :HA significantly reduced the inflammatory cytokine induced target IGFBP3 in the D + IFNα + HA group (2.85 ± 0.75%) by 93.1% compared to the D group (41.22 ± 2.58%) and by 94.6% compared to the D + IFNα group (52.52 ± 3.83%) (Fig. 4D). In combination with previously published insights correlating decreased levels of IGFBP3 with decreased apoptosis [39,40], this data indirectly suggests that HA may act as anti-apoptotic biomolecule. To assess the pro-apoptotic effect induced under IFNα2β signaling, we tested the protein expression of active caspase 3 fragment p17.
Impact of the IGFBP3 A-202C polymorphism on susceptibility and clinicopathologic features of breast cancer
2015, Biomedicine and PharmacotherapyTobacco specific carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone suppresses a newly identified anti-tumor IGFBP-3/IGFBP-3R system in lung cancer cells
2013, Lung CancerCitation Excerpt :Lower IGFBP-3 levels in the circulation has been shown to be associated with a greater risk of common cancers such as lung, breast, prostate, and colorectal cancer [25–32], while inverse correlation of IGFBP-3 with cancer risk has been detected only after IGFBP-3 is adjusted to IGF-1 level [33]. Nonetheless, the involvement of IGFBP-3 in cell growth inhibition and induction of apoptosis in lung, breast, prostate, and colon cancer has been demonstrated in vivo and in vitro [34–41]. IGFBP-3 has been known to exert its anti-tumor effects IGF-dependently as well as independently.
A novel antitumor activity of deguelin targeting the insulin-like growth factor (IGF) receptor pathway via up-regulation of IGF-binding protein-3 expression in breast cancer
2013, Cancer LettersCitation Excerpt :Furthermore, the anti-apoptotic properties of IGF-1R confer the resistance to chemotherapy and radiotherapy for cancer cells. The overexpression of the IGF-1R has been observed in most breast cancer cell lines regardless of their ER status and estrogen responsiveness [20] and in a large series of human tissue specimens [21,22]. These findings provide a rationale for targeting IGF-1R as an anticancer therapeutic strategy.
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Corresponding author. Lady Davis Research Institute, 3755 Cote Ste Catherine Road, Montreal, Quebec, Canada H3T 1E2. Fax: (514) 340-7502. E-mail: [email protected].