Peri/nuclear localization of intact insulin-like growth factor binding protein-2 and a distinct carboxyl-terminal IGFBP-2 fragment in vivo

Insulin-like growth factor binding protein-2 is a novel mediator of p53 inhibition of insulin-like growth factor signaling

“…IGF-independent activities of IGFBP-2 have been suggested by its interactions with α5β1-integrin, 40 its cytosolic uptake, 41 and its nuclear translocation. 42,43 Although IGFBP-2 has been shown to inhibit proliferation in multiple cell lines in IGF-dependent cell culture systems, 41 experimentally created IGFBP-2 overexpression in vitro increased invasiveness of ovarian 44 and bladder 45 cancer cell lines, and increased proliferation of Y-1 murine adrenocortical tumor cells 46 and DU145 prostate cancer cells. 47 IGFBP-2 expression has been shown to be elevated in multiple tumors (including prostate, colon, adrenocortical, mammary, ovarian, brain, thyroid, and hepatic cancers), to often correlate positively with tumor grade and/or stage and to be increased in the serum of these patients.…”

Insulin-Like Growth Factor Binding Protein-2: A Possible Regulator of Invasive Growth in Glioblastoma

“…Therefore, interaction between integrins and IGFBP2, cleavage of IGFBPs by proteases, and other factors that could influence the affinity of IGFBP2 for IGFs may be important regulatory mechanisms of pericellular IGF function. On the other hand, IGFBP2 has also been reported in several studies to have a cytosolic or perinuclear localization, suggesting that IGFBP2 may also have IGF-independent functions (Hoeflich et al, 2004;Migita et al, 2010). IGFBP2 knockout mice are both viable and fertile, and do not show significant differences in prenatal or postnatal body growth (Wood et al, 1993(Wood et al, , 2000.…”

Primary pigmented nodular adrenocortical disease reveals insulin-like growth factor binding protein-2 regulation by protein kinase A

“…IGF-independent actions of the IGFBPs are also coming to light [34]. Intracellular functions of IGFBP-2 are suggested by its cytosolic uptake by colon carcinoma cell lines [35], nuclear translocation in hyperoxia (95% O 2 ) exposed lung adenocarcinoma cell line [36], and isolation in the peri/nuclear fractions of tissues from IGFBP-2 transgenic and non-transgenic mice [37].…”