v-mil induces autocrine growth and enhanced tumorigenicity in v-myc-transformed avian macrophages |
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Authors: | T Graf F von Weizsaecker S Grieser J Coll D Stehelin T Patschinsky K Bister C Bechade G Calothy A Leutz |
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Institution: | 1. State Key Laboratory of Holistic Integrative Management of Gastrointestinal Cancers, Department of Pathology, Xijing Hospital and School of Basic Medicine, Fourth Military Medical University, Xi''an, China;2. Department of Pathology, Baotou Medical college, Baotou, Inner Mongolia Autonomous Region, China;3. Department of Hematology, Xijing Hospital, Fourth Military Medical University, Xi''an, China;4. Department of Pathology, The First Affiliated Hospital of University of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China |
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Abstract: | MH2, an avian retrovirus containing the v-myc and v-mil oncogenes, rapidly transforms chick hematopoietic cells in vitro. The transformed cells belong to the macrophage lineage and proliferate in the absence of exogenous growth factors. Here we analyze a series of MH2 deletion mutants and show that these two oncogenes together establish an autocrine growth system in which v-myc stimulates cell proliferation, while v-mil induces the production of chicken myelomonocytic growth factor (cMGF). We also demonstrate that these two oncogenes cooperate in vivo. MH2 efficiently induces monocytic leukemias and liver tumors, while deletion mutants lacking either a functional v-mil or v-myc do not. |
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