Midkine induces the transformation of NIH3T3 cells

Kadomatsu, Kenji; Hagihara, Mao; Akhter, Shafinaz; Fan, Qi‐Wen; Muramatsu, Hisako; Muramatsu, Takashi

doi:10.1038/bjc.1997.58

Cited by 138 publications

(119 citation statements)

References 35 publications

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“…Cancerrelated activities of MK have been reported by many laboratories. These activities include transforming, migrating, fibrinolytic, mitogenic, antiapoptotic, and angiogenic ones (Kojima et al, 1995;Choudhuri et al, 1997;Kadomatsu et al, 1997;Qi et al, 2000Qi et al, , 2001. Furthermore, we recently succeeded in suppressing tumour growth by using antisense MK oligodeoxyribonucleotide (Takei et al, 2001(Takei et al, , 2002.…”

Section: Discussionmentioning

confidence: 99%

Correlation of elevated level of blood midkine with poor prognostic factors of human neuroblastomas

et al. 2003

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The heparin-binding growth factor midkine (MK) is the product of a retinoic acid-responsive gene, and is implicated in neuronal survival and differentiation, and carcinogenesis. We previously reported that MK mRNA expression is elevated in neuroblastoma specimens at all stages, whereas pleiotrophin, the other member of the MK family, is expressed at high levels in favourable neuroblastomas. As MK is a secretory protein, it can be detected in the blood. Here, we show a significant correlation of the plasma MK level with prognostic factors of neuroblastomas. The plasma MK level was determined in 220 patients with neuroblastomas, and compared with that in children without malignant tumors (n ¼ 17, o500 pg ml À1 ). The plasma MK level became significantly elevated with advancing stages (stage 1: 445 pg ml À1 (median), n ¼ 73; stage 2: 589, n ¼ 39; stage 3: 864, n ¼ 40; stage 4: 1445, n ¼ 56; and stage 4S: 2439, n ¼ 12). More importantly, a higher MK level was strongly correlated with poor prognostic factors: over 1 year of age (P ¼ 0.0299), MYCN amplification (Po0.0001), low TrkA expression (P ¼ 0.0005), nonmass screening, sporadic neuroblastomas (Po0.0001), and diploidy/tetraploidy (P ¼ 0.0007). Thus, these results demonstrate that the plasma MK level is a good marker for evaluating the progression of neuroblastomas. Moreover, considering the ability of antisense MK oligodeoxyribonucleotide to suppress tumour growth of colorectal carcinoma cells in nude mice, as recently reported, the present study suggests that MK is a possible candidate molecular target for therapy for neuroblastomas.

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Section: Discussionmentioning

confidence: 99%

Correlation of elevated level of blood midkine with poor prognostic factors of human neuroblastomas

et al. 2003

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“…Western blot analysis was performed as described previously. 37 Briefly, we separated the samples by 10% SDS-PAGE and then transferred them to a nitrocellulose membrane (Whatman, Florham Park, NJ). We blocked the membranes with 5% (w/v) dry fat-free milk in PBS with 0.1% Tween for 60 minutes at room temperature.…”

Section: Western Blot Analysismentioning

confidence: 99%

Basigin/CD147 Promotes Renal Fibrosis after Unilateral Ureteral Obstruction

Kato

Kosugi

Sato

et al. 2011

The American Journal of Pathology

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Regardless of their primary causes, progressive renal fibrosis and tubular atrophy are the main predictors of progression to end-stage renal disease. Basigin/ CD147 is a multifunctional molecule-it induces matrix metalloproteinases and hyaluronan, for example-and has been implicated in organ fibrosis. However, the relationship between basigin and organ fibrosis has been poorly studied. We investigated basigin's role in renal fibrosis using a unilateral ureteral obstruction model. Basigin-deficient mice (Bsg ؊/؊ ) demonstrated significantly less fibrosis after surgery than Bsg ؉/؉ mice. Fewer macrophages had infiltrated in Bsg ؊/؊ kidneys. Consistent with these in vivo data, primary cultured tubular epithelial cells from Bsg ؊/؊ mice produced less matrix metalloproteinase and exhibited less motility on stimulation with transforming growth factor ␤. Furthermore, Bsg ؊/؊ embryonic fibro blasts produced less hyaluronan and ␣-smooth muscle actin after transforming growth factor ␤ stimulation. Together, these results demonstrate for the first time that basigin is a key regulator of renal fibrosis. Basigin could be a candidate target molecule for the prevention of organ fibrosis.

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“…(5)(6)(7)(8) Moreover, since both molecules promote cell growth and survival, as well as angiogenesis, it has been suggested that they are involved in carcinogenesis, which is supported by their increased expression in several types of tumors, including osteosarcoma. (9)(10)(11)(12)(13)(14)(15) To analyze the role of Mdk and Ptn in vivo, mouse deficiency models for both genes have been generated. (16)(17)(18) Not necessarily expected, neither the Mdk-nor the Ptn-deficient mice displayed major abnormalities, although a more detailed analysis has demonstrated a role of both molecules in hippocampus development, behavior, and learning.…”

Section: Introductionmentioning

confidence: 99%

Increased trabecular bone formation in mice lacking the growth factor midkine

Neunaber

Catalá-Lehnen

Beil

et al. 2010

Journal of Bone and Mineral Research

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Midkine (Mdk) and pleiotrophin (Ptn) comprise a family of heparin-binding growth factors known primarily for their effects on neuronal cells. Since transgenic mice overexpressing Ptn have been reported to display increased bone density, we have previously analyzed Ptndeficient mice but failed to detect any abnormality of skeletal development and remodeling. Together with the finding that Mdk expression increases in the course of primary osteoblast differentiation, we reasoned that Mdk, rather than Ptn, could play a physiologic role in bone formation. Here, we show that Mdk-deficient mice display an increased trabecular bone volume at 12 and 18 months of age, accompanied by cortical porosity. Histomorphometric quantification demonstrated an increased bone-formation rate compared with wild-type littermates, whereas bone resorption was differentially affected in trabecular and cortical bone of Mdk-deficient mice. To understand the effect of Mdk on bone formation at the molecular level, we performed a genome-wide expression analysis of primary osteoblasts and identified Ank and Enpp1 as Mdk-induced genes whose decreased expression in Mdk-deficient osteoblasts may explain, at least in part, the observed skeletal phenotype. Finally, we performed ovariectomy and observed bone loss only in wild-type but not in Mdk-deficient animals. Taken together, our data demonstrate that Mdk deficiency, at least in mice, results in an increased trabecular bone formation, thereby raising the possibility that Mdk-specific antagonists might prove beneficial in osteoporosis therapy. ß

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Midkine induces the transformation of NIH3T3 cells

Cited by 138 publications

References 35 publications

Correlation of elevated level of blood midkine with poor prognostic factors of human neuroblastomas

Correlation of elevated level of blood midkine with poor prognostic factors of human neuroblastomas

Basigin/CD147 Promotes Renal Fibrosis after Unilateral Ureteral Obstruction

Increased trabecular bone formation in mice lacking the growth factor midkine

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