PubMed · 8488332
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B Barbaro, A De Franco. 1993. [Rectal neoplasms].. https://pubmed.ncbi.nlm.nih.gov/8488332/
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The G12 subfamily of heterotrimeric G proteins, comprised of the alpha-subunits Galpha12 and Galpha13, has been implicated as a signaling component in cellular processes ranging from cytoskeletal changes to cell growth and oncogenesis. In an attempt to elucidate specific roles of this subfamily in cell regulation, we sought to identify molecular targets of Galpha12. Here we show a specific interaction between the G12 subfamily and the cytoplasmic tails of several members of the cadherin family of cell-surface adhesion proteins. Galpha12 or Galpha13 binding causes dissociation of the transcriptional activator beta-catenin from cadherins. Furthermore, in cells lacking the adenomatous polyposis coli protein required for beta-catenin degradation, expression of mutationally activated Galpha12 or Galpha13 causes an increase in beta-catenin-mediated transcriptional activation. These findings provide a potential molecular mechanism for the previously reported cellular transforming ability of the G12 subfamily and reveal a link between heterotrimeric G proteins and cellular processes controlling growth and differentiation.
BACKGROUND: Telomerase in an enzyme ribonucleoprotein responsible for cell immortality and oncogenesis. Telomerase activity has been detected in most cancers, including prostate cancer. To verify whether the detection of telomerase in prostate needle biopsy samples could have diagnostic value, we blindly assayed telomerase activity in samples from patients who were clinically suspected of having prostate cancer. METHODS: A total of 183 prostate biopsy samples was obtained from 63 patients who were suspected of having prostate cancer. Telomerase activity was determined by polymerase chain reaction (PCR)-based telomeric repeat amplification protocol (TRAP) assay. An internal telomerase assay standard (ITAS) was used in this study to distinguish false negatives. RESULTS: Telomerase activity was detected in 17 of 19 (89.5%) patients with prostate cancer (chi(2) test, P < 0.005). In 39 of 42 (92.9%) biopsy samples from these 19 prostate cancer patients, confirmed histologically as prostate cancer, telomerase activity (chi(2) test, P < 0.005) was detected. Meanwhile, we also found one false-positive sample. In contrast, all of 44 normal or benign prostate disease patients (124 biopsy specimens) were telomerase-negative. We also revealed that poorly differentiated prostate cancer often expresses a high level of telomerase activity. The area of cancer tissue in biopsy specimens was not associated with relative telomerase activity. CONCLUSIONS: This study suggests that determination of telomerase activity in prostate needle-biopsy samples might be a useful tool for detecting prostate cancer.
BACKGROUND: Angiogenesis is important for prostate organogenesis and prostate cancer progression. It is not yet known whether androgens promote part of their control of prostate structure and function by influencing angiogenesis. The aim of this study was to explore the possible androgenic regulation of the angiogenic factor vascular endothelial growth factor (VEGF) and its receptors flt-1 and flk-1/KDR in the rat ventral prostate (VP) and Dunning R3327 PAP adenocarcinoma. METHODS: RNA was prepared from VP and tumors of intact and castrated rats. VEGF, flt-1, and flk-1/KDR mRNA levels were determined using competitive RT-PCR. RESULTS: VEGF121, VEGF165, and VEGF189 together with flt-1 and flk-1/KDR mRNA were detected. The VEGF, but not flt-1 mRNA levels were significantly decreased in the VP after castration. The Dunning tumor expressed high levels of mRNA for VEGF and its receptors compared to the VP. The flt-1 mRNA level in the tumor increased after castration, while the VEGF mRNA levels were unchanged. CONCLUSIONS: Decreased mRNA expression of VEGF, but not flt-1, was found in the rat VP after castration. However, in the Dunning tumor, castration did not alter the expression of VEGF mRNA. Moreover, elevated levels of both mRNA for VEGF and its receptors relative to the VP were observed, indicating that the VEGF system may be important for Dunning tumor development.