Correlation between tumor induction and the large external transformation sensitive protein on the cell surface (original) (raw)
Related papers
Journal of Virology, 1986
We have compared the capacities of the E1A regions of nononcogenic adenovirus type 5 (Ad5) and highly oncogenic Ad12 to cooperate with the EJ bladder carcinoma Ha-ras-1 oncogene in the transformation of primary baby rat kidney cells. Both E1A regions, when cotransfected with the Ha-ras oncogene, transformed the primary cells with a low frequency. Ad5 E1A plus Ha-ras-transformed cells differed in phenotype from cells transformed by Ad12 E1A plus Ha-ras. The cells expressing Ad5 E1A appeared highly transformed and practically failed to adhere to plastic. This phenotype may be due to the virtually complete absence of fibronectin gene expression in these cells. In contrast, the cells expressing Ad12 E1A were flatter and adhered to plastic, whereas fibronectin gene expression was reduced but not absent. The oncogenic potential of the two types of E1A plus ras-transformed cells was tested by their injection into both athymic nude mice and weanling syngeneic rats. The Ad5 E1A plus ras-tran...
Detection of the large external transformation-sensitive protein on some epithelial cells
Experimental Cell Research, 1977
The large, external, transform&ion-sensitive (LETS) protein is detected on the surface of epitbeiial cells. Whereas fibroblasts build a massive network of fibrillar LETS protein in one-week-old confluent culture, epithelial cells do not. This observation may be useful for distinguishing epithelial cells from fibroblasts. When rat liver epitbelial cells are continuously passaged in culture, surface LETS protein undergoes a significant alteration first from fibrillar organization to patchlike, then to complete absence.
Cell, 1977
Six independently isolated adenovirus P-transformed rat cell lines and one adenovirus 54ransformed human cell line have been examined in vitro for serum growth requirements, saturation density, anchorage-independent growth, proteolytic enzyme activity and the presence of LETS glycoprotein and T antigen. This series of adenovirus-transformed cell lines exhibits an oncogenic spectrum ranging from being tumorigenic in immunocompetent rats through to nontumorigenic in adult nude mice. The relevance of the in vitro findings to growth potential in vivo is discussed.
1987
Fujinami sarcoma virus (FSV) encodes a protein-tyrosine kinase, pl.W"*1'"1, whose enzymatic activity and ability to transform cultured cells to a neoplastic phenotype are reduced by substitution of the major autophosphorylation site tyrosine-1073 with other amino acids. We com pared the histopathology of tumors formed in syngeneic immunocompetent rats by Rat-2 cells and by Rat-2 cells transformed in culture with (a) wild type (wt) FSV, (b) mutant FSV where the codon for tyrosine-1073 of pl.W"B"'~had been changed to codons for phenylalanine or serine, and (c) a revertan! FSV, genotypically identical to wt FSV, in which the codon for tyrosine-1073 had been restored. Latency periods from cell inoculation to tumor formation were 12-29 weeks with Rat-2
Tumorigenicity of cells transformed by adenovirus type 12 by evasion of T-cell immunity
1983
Evidence is presented that cells transformed by adenovirus type 12 are oncogenic because they escape from T-cell immunity. This effect is brought about by reducing the expression of class I transplantation antigens and is a function of the protein translated from the 13S mRNA, transcribed from early region la. These findings establish a novel mechanism by which transformed cells can acquire an oncogenic phenotype. ADENOvIRUS-transformed rodent cells exhibit variable degrees of oncogenicity, depending on the adenovirus species used for transformation: rat cells transformed by the highly oncogenic adenovirus 12 (Ad12) are highly oncogenic in the syngeneic host', whereas rat cells transformed by the nononcogenic adenoviruses, for example Ad2 and Ad5, are rarely tumorigenic in immunocompetent syngeneic rats2. It has been proposed that cells transformed by the non-oncogenic adenoviruses fail to form tumours because they are more antigenic than are cells transformed by oncogenic adenoviruses and
The Journal of Cell Biology, 1979
Fibronectin (FN; also called large external transformation-sensitive [LETS] protein or cell-surface protein [CSP]) is a large cell-surface glycoprotein that is frequently observed to be either absent or greatly reduced on the surfaces of malignant cells grown in vitro. Because FN may be a useful molecular marker of cellular malignancy, we have carried out an extensive screening to test the specific association among the degree of expression of FN, anchorage-independent growth, and tumorigenicity in the athymic nude mouse. A variety of diploid cell strains and established cell lines were tested for the expression of surface FN by indirect immunofluorescence using rabbit antisera against human cold insoluble globulin, rodent plasma FN, or chicken cell-surface FN. Concomitantly, the cells were assayed for tumor formation in nude mice and for the ability to form colonies in methylcellulose. Tumorigenic cells often showed very low surface fluorescence, confirming earlier reports. However...
Tumori Journal, 1990
The purpose of the study was to determine whether the selection by adhesion to fibronectin (FN) also selects for cells with different tumorigenic and metastatic abilities. M3 murine mammary adenocarcinoma cells with moderate metastatic potential were seeded on FN-coated plastic substrates. Non-adherent cells were removed at 30 min, and the adherent ones were expanded in monolayer culture. Selected tumor cells were then harvested and inoculated sc into syngeneic mice. The selection procedure was repeated three times. After the third cycle, tumors were further maintained by sc trocar transplantation, and the variant obtained was called M3Ad. Although the in vitro selection was adhesion to FN substrate, the in vitro adhesion behavior of the variant M3Ad was identical to that of the parental tumor M3. However, the cytogenetic profile and the in vivo behavior indicated that M3Ad differed from M3. The distribution of the chromosome number of M3Ad cells revealed a lower mode and mean than ...
Adenovirus type 12 E1B 19-kilodalton protein is not required for oncogenic transformation in rats
Journal of Virology, 1988
The adenovirus type 12 mutants in700 and pm700 carry site-specific mutations within the reading frame encoding the E1B 19-kilodalton protein (19K protein) which prevent the production of the intact 19K protein. In cultures of human A549 cells, these mutants grow just as well as the wild-type virus does, but they display a large-plaque (lp), cytocidal (cyt) phenotype. DNA in these infected cells is not degraded, but at late times in human KB cells infected by the mutants, the mutants display a DNA degradation (deg) phenotype. The transformation phenotype of these mutants is also host range. Although the mutants are defective for transformation of the 3Y1 rat cell line, they transform rat and mouse primary kidney cells in vitro at wild-type efficiency and are capable of inducing tumors in rats. These results support the view that the type 12 E1B 19K protein is not obligatory for oncogenic transformation.
Journal of Virology, 1994
Chimeric adenovirus type 5 (Ad5)/Ad12 early region 1A (E1A) genes were used to transform primary baby rat kidney cells in cooperation with Ad12 E1B, and the resulting cell lines were assayed for tumorigenicity in syngeneic rats. It was found that lines were nontumorigenic when transformed by hybrid E1A genes consisting of the amino-terminal 80 amino acids from Ad12 including conserved region 1 (CR1), with the remaining portion from Ad5. In contrast, cell lines transformed by hybrids containing Ad12 E1A sequences from the amino terminus to the leftmost border of CR3 or beyond were tumorigenic. To extend these results, sequences spanning CR2 and CR3 of Ad5 E1A were replaced with the homologous regions of Ad12 E1A and additional transformed cell lines were established. These lines were weakly-to-moderately tumorigenic, suggesting that Ad12 E1A sequences between CR2 and CR3 may be involved in tumorigenicity but are not the sole factors influencing it. Interestingly, examination of an E1...
Biochemistry (Moscow). Supplement. Series A, Membrane and cell biology, 2017
⎯The abilities of tumor cells to invade and metastasize are frequent causes of death of cancer patients. Studying the mechanisms of cell motility alterations and acquisition of enhanced metastatic potential as the result of transformation is an important aspect in current cell biology. The initial and determinant step of cell motility is the formation of active cell edge with protrusions based on the Arp2/3-dependent actin polymerization. We used three different cell systems as examples of different models of tumor transformation to study the alteration and redistribution of protrusive activity caused by transformation in fibroblasts. We analyzed relationships between detected alterations and the acquisition of increased invasive potential by cells. Active edge of untransformed fibroblasts occupies about 50% of the cell perimeter and is concentrated at the cell front. There are well pronounced stable regions at the lateral cell edges. Tumor transformation causes redistribution of protrusive activity of fibroblasts irrespective of their origin and the nature of transforming agents. The length of active edges significantly increases, up to 92% of the total perimeter in fibrosarcoma cells of tumor origin. These cells have practically no stable edges. The intensity of protrusive activity of transformed cells is also increased. Single transformed cells show a decrease in the directionality and rate of migration on 2D substrate without special stimulation. Instead, they gain the capacity to migrate in 3D and to invade matrigel. These abilities increase in parallel with the intensification of edge activity. We showed that invasive abilities are not associated with the activation of matrix metalloproteinases in the studied cell systems. Our data demonstrate that the increase of length of active edge could be considered as an additional feature of cell transformation together with the reduction of stress fiber and focal adhesions and that the excessive protrusive activity results in the development of explorative migration of tumor cells.