PMID- 1543541 OWN - NLM STAT- MEDLINE DCOM- 19920416 LR - 20191021 IS - 0899-1987 (Print) IS - 0899-1987 (Linking) VI - 5 IP - 1 DP - 1992 TI - Alterations in mRNA levels for growth-related genes after transplantation into castrated hosts in oncogene-induced clonal mouse prostate carcinoma. PG - 52-61 AB - A clonal mouse prostate carcinoma was established by the introduction of the ras and myc oncogenes via the recombinant retrovirus Zipras/myc 9 using a mouse prostate reconstitution model system. A single-cell suspension derived from an early passage ras+myc-induced carcinoma was inoculated into the flanks of intact or castrated adult male C57BL/6 mice, and tumors were harvested 3 wk postinoculation for northern and Southern blotting. Tumor volume analysis showed that this carcinoma was not dependent on testicular androgens for growth. Southern blot analysis of virus-cell DNA junction fragments revealed that tumor cell populations recovered from both intact and castrated mice were progeny of the same virus-infected cell. Northern blotting showed that mRNA levels for the four growth-related genes transforming growth factor-beta 1 (TGF-beta 1), transforming growth factor-beta 3 (TGF-beta 3), tissue-type plasminogen activator (tPA), and c-myc were significantly elevated in clonal mouse prostate carcinomas grown in castrated hosts. In contrast, androgen receptor mRNA levels were significantly reduced under the same conditions. The response of TGF-beta 1, tPA, and c-myc mRNA levels in the carcinomas grown in castrated hosts was similar to that shown previously in normal rat ventral prostate. However, unlike normal rat ventral prostate after castration, increased numbers of apoptotic cells were not seen in the castrated group relative to the intact group at the time of analysis, indicating that the altered gene expression was not associated with cell death. In addition, testosterone-repressed prostate mRNA number 2 levels, shown previously to be elevated after castration in normal rat ventral prostate, were not increased in the androgen-deprived clonal mouse prostate carcinomas. Therefore, this early passage clonal ras+myc-induced prostate carcinoma demonstrates unique patterns of expression for a set of growth-related genes in an androgen-deprived environment. FAU - Egawa, S AU - Egawa S AD - Scott Department of Urology, Baylor College of Medicine, Houston, TX 77030. FAU - Kadmon, D AU - Kadmon D FAU - Miller, G J AU - Miller GJ FAU - Scardino, P T AU - Scardino PT FAU - Thompson, T C AU - Thompson TC LA - eng GR - CA-50588/CA/NCI NIH HHS/United States PT - Journal Article PT - Research Support, U.S. Gov't, Non-P.H.S. PT - Research Support, U.S. Gov't, P.H.S. PL - United States TA - Mol Carcinog JT - Molecular carcinogenesis JID - 8811105 RN - 0 (Androgens) RN - 0 (RNA, Messenger) RN - 0 (RNA, Neoplasm) RN - 0 (Receptors, Androgen) RN - 0 (Transcription Factors) RN - 0 (Transforming Growth Factor beta) RN - EC 3.4.21.68 (Tissue Plasminogen Activator) RN - EC 3.4.21.73 (Urokinase-Type Plasminogen Activator) SB - IM MH - Androgens/physiology MH - Animals MH - Clone Cells MH - Gene Expression Regulation, Neoplastic MH - Genes, fos MH - Genes, jun MH - Genes, myc MH - Genes, ras MH - Male MH - Mice MH - Oncogenes MH - Orchiectomy MH - Prostatic Neoplasms/*genetics/pathology MH - Proto-Oncogenes MH - RNA, Messenger/genetics MH - RNA, Neoplasm/genetics MH - Receptors, Androgen/genetics MH - Tissue Plasminogen Activator/genetics MH - Transcription Factors/genetics MH - Transforming Growth Factor beta/genetics MH - Tumor Cells, Cultured MH - Urokinase-Type Plasminogen Activator/genetics EDAT- 1992/01/01 00:00 MHDA- 1992/01/01 00:01 CRDT- 1992/01/01 00:00 PHST- 1992/01/01 00:00 [pubmed] PHST- 1992/01/01 00:01 [medline] PHST- 1992/01/01 00:00 [entrez] AID - 10.1002/mc.2940050110 [doi] PST - ppublish SO - Mol Carcinog. 1992;5(1):52-61. doi: 10.1002/mc.2940050110.