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A relation was studied between body weight measured at the age of 3, 6 and 12 months in Polish Holstein-Friesian (HF) heifers (n=111) and young bulls (n=87) and C/T polymorphism within intron IV of bovine osteopontin encoding gene (SPP1). Three half-sib (HS) families were considered, each sired by heterozygous C/T sire. Significant association was found of SPP1 C>T SNP with body Wright in all the analysed HS progeny groups of young heifers and bulls. Within young bulls the differences were identified (P≤0.05) in body weight between the SPP1 genotypes (8514C/C, 8514C/T, 8514T/T) in month 3, 6 and 12 of age. Within heifers, however, the differences (P≤0.05) were found in the progeny groups aged 6 and 12 months. Moreover, when data from bulls and heifers were pooled (n=198) the highly significant effect (P≤0.01) of SPP1 genotype on body weight was observed at the age of 6 and 12 months.
Osteopontin (OPN) is a secreted, non-collagenous, sialic acid-rich protein which functions by mediating cell-matrix interactions and cellular signaling via binding with integrins and CD44 receptors. An increasing number of studies have shown that OPN plays an important role in controlling cancer progression and metastasis. OPN was found to be expressed in many human cancer types, and in some cases, its over-expression was shown to be directly associated with poor patient prognosis. In vitro cancer cell line and animal model studies have clearly indicated that OPN can function in regulating the cell signaling that ultimately controls the oncogenic potential of various cancers. Previous studies in our laboratory demonstrated that OPN is highly expressed in human osteosarcoma (OS) cell line OS-732. In this study, we successfully reduced the tumorigenecity of OS-732 cells xenotransplanted into nude mice, using the antisense human OPN (hOPN) RNA expression vector.
Malignant tumors are characterized by dysregulated cell growth and the metastasis of secondary tumors. Numerous studies have documented that osteopontin (OPN) plays a key role in regulating tumor progression and metastasis. Here, we show that the overexpression of OPN in human embryo kidney-293 cells significantly increases both the level of cell proliferation, by provoking the G1/S transition, and the level of cell migration in vitro. These findings suggest that augmented OPN contributes to cell growth and motility. Inhibiting OPN or the pathway it stimulates may therefore represent a novel approach for the treatment of primary tumors and associated metastases.
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