PubMed · 7961365
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P Bracke, B Corthouts. 1994. Multiple intraperitoneal hematomas.. https://pubmed.ncbi.nlm.nih.gov/7961365/
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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.
Cancers of the microsatellite mutator phenotype (MMP) show exaggerated genomic instability at simple repeat sequences. More than 50 percent (21 out of 41) of human MMP+ colon adenocarcinomas examined were found to have frameshift mutations in a tract of eight deoxyguanosines [(G)8] within BAX, a gene that promotes apoptosis. These mutations were absent in MMP- tumors and were significantly less frequent in (G)8 repeats from other genes. Frameshift mutations were present in both BAX alleles in some MMP+ colon tumor cell lines and in primary tumors. These results suggest that inactivating BAX mutations are selected for during the progression of colorectal MMP+ tumors and that the wild-type BAX gene plays a suppressor role in a p53-independent pathway for colorectal carcinogenesis.
HLA class I restriction and tumor specificity of cytotoxicity in the IL-2-activated tumor-infiltrating lymphocytes from 16 patients with non-small cell lung cancer were investigated. Six HLA class I-restricted and tumor-specific CTL lines were established: (i) HLA A2-restricted and adenocarcinoma-specific CTLs in three (two A0201+ and one A0206+) patients with adenocarcinoma, (ii) HLA A3101- and A3302-restricted and adenocarcinoma-specific CTLs in an HLA A3101/3302+ patient with adenocarcinoma, and (iii) HLA A3302-restricted CTLs and (iv) HLA A2402-restricted CTLs recognizing tumors with different types of histology in an HLA A3302+ patient with adenocarcinoma and an HLA A2402+ patient with squamous cell carcinoma (SCC), respectively. The three HLA A2-restricted CTL lines recognized 4, 4, or 6 of 15 HLA A2+ adenocarcinoma cell lines that originated from lung, stomach, colon, and breast with different subtypes (HLA A0201, A0206, and A0207), respectively. Furthermore, the CTLs of an HLA A0206+ patient recognized five different fractions of peptides eluted from an HLA A0201+ adenocarcinoma cell line. These results showed evidence of the existence of HLA class I-restricted and tumor-specific CTLs recognizing peptide antigens on HLA-A alleles of adenocarcinoma or SCC in tumor sites of a substantial number of patients with non-small cell lung cancer.