Overexpression of autocrine motility factor receptor (AMFR) in NIH3T3 fibroblasts induces cell transformation |
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| Authors: | Onishi Yasuharu Tsukada Kazuhiro Yokota Jun Raz Avraham |
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| Affiliation: | (1) Tumor Progression and Metastasis Program, Karmanos Cancer Institute, Detroit, Michigan, USA;(2) Second Department of Surgery, Faculty of Medicine, Toyama Medical and Pharmaceutical University, Toyama, Japan;(3) Biology Division, National Cancer Center Research Institute, Tokyo, Japan;(4) Department of Pathology and Radiation Oncology, Wayne State University School of Medicine, Detroit, Michigan, USA |
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| Abstract: | Autocrine motility factor receptor (AMFR) is a cell surface glycoprotein of 78000 molecular weight (gp78), regulating cell motility signaling in vitro and metastasis in vivo. To test whether AMFR could be a common mediator of transformation and oncogenic itself, we transfected NIH3T3 fibroblast cells with expression vectors carrying the full-length cDNA for mouse AMFR and evaluated the effects of increased AMFR on transforming potential. The cells stably expressing high levels of AMFR as a result of transfection displayed a complete morphological change and acquired the ability to grow even in low serum. Furthermore, they were anchorage-independent for growth in soft agar and more motile in phagokinetic track assay. Interestingly, the enhanced expression of AMFR produced tumors in nude mice. Our findings provide a direct evidence that overexpression of the AMFR is associated with the acquisition of a transformation phenotype. |
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| Keywords: | motility transformation tumorigenicity phosphohexose isomerase |
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