Overexpression of autocrine motility factor receptor (AMFR) in NIH3T3 fibroblasts induces cell transformation

• Published in: Clinical & experimental metastasis Vol. 20; no. 1; pp. 51 - 58
• Main Authors: Onishi, Yasuharu, Tsukada, Kazuhiro, Yokota, Jun, Raz, Avraham
• Format: Journal Article
• Language: English
• Published: Netherlands Springer Nature B.V 2003
• Subjects: 3T3 Cells; Animals; Cell Division; Cell Movement; Cell Transformation, Neoplastic; Female; Fibroblasts - metabolism; Mice; Mice, Nude; Neoplasm Transplantation; Neoplasms, Experimental - etiology; Receptors, Autocrine Motility Factor; Receptors, Cytokine - metabolism; Time Factors; Transfection; Ubiquitin-Protein Ligases
• ISSN: 0262-0898; 1573-7276
• DOI: 10.1023/a:1022594503657

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.