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Gene Review

10T  -  DNA segment, 10T

Mus musculus

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Disease relevance of 10T


High impact information on 10T

  • In a study of the relation between chronic inflammation and carcinogenesis, C3H mouse fibroblasts of the 10T 1/2 clone 8 line (10T 1/2 cells) were exposed to human neutrophils stimulated to synthesize reactive oxygen intermediates or to a cell-free enzymatic system generating superoxide (xanthine oxidase plus hypoxanthine) [5].
  • The mechanism of in vitro transformation of the mouse embryo fibroblast C3H/10T 1/2 clone 8 by aflatoxin B1 (AFB1) was studied in confluent holding (CH) experiments [6].
  • Thus the addition of ECDGF, the phorbol ester TPA, protein kinase C or phosphoinositidase C to crude membranes prepared from C3H 10T 1/2 cells resulted in the enhanced phosphorylation of this protein [7].
  • While TGF-beta 1 inhibited DNA synthesis in 10T 1/2 cells and a nonmetastatic tumor, cells with intermediate to high metastatic ability were stimulated up to 5.8-fold by TGF-beta 1 [8].
  • Cell lines with varying tumorigenic and metastatic potentials have been obtained by transformation of 10T 1/2 fibroblasts using radiation or transfection with T-24 H-ras [8].

Biological context of 10T

  • In serum-supplemented media, methylcholanthrene-transformed C3H/10T 1/2 CL8 cells exhibit various aspects of the transformed phenotype such as irregular morphology, extensive cell overlap, lack of density-dependent inhibition of division, a saturation density of 1.1 X 10(5) cells/sq cm and tumorigenicity in vivo [9].
  • Partial down-regulation of protein kinase C in C3H 10T 1/2 mouse fibroblasts transfected with the human Ha-ras oncogene [10].
  • While 10T 1/2 cells tended to be somewhat more heat resistant than were any of their transformed counterparts, this depended upon cell density (or state of growth) during heating [2].
  • Effect of formation and removal of aflatoxin B1:DNA adducts in 10T 1/2 mouse embryo fibroblasts on cell viability [11].
  • The nature of the BaP water-soluble derivatives produced by the C3H/10T 1/2 and CVP cell lines was investigated by hydrolysis of culture medium with beta-glucuronidase and arylsulfatase [12].

Anatomical context of 10T

  • The intracellular profile of organic soluble metabolites produced by both cell lines consisted predominantly of BaP phenolic derivatives and was qualitatively similar to the spectrum of metabolites produced by the incubation of BaP with C3H/10T 1/2 or CVP cell microsomes [12].
  • C3H/10T 1/2 cells were induced to differentiate into muscle cells by treatment with 5-azacytidine, and the effects of tumor promoters, nonpromoters, and inhibitors of tumor promotion on this induced differentiation were investigated [13].
  • Residual keratin 1/10T clumps were located in the cell periphery and at desmosomes which maintained a normal architecture [14].
  • In contrast, small but statistically significant reductions in NAb binding were observed following v-H-ras transformation of NIH 3T3 cells or v-src transformation of 10T 1/2 [15].
  • 10T mice have higher serum and skeletal IGF-I, greater trabecular bone volume fraction, more trabeculae, and a higher number of osteoclasts at 16 wk, compared with B6 (P < 0.05) [16].

Associations of 10T with chemical compounds

  • Mutagenicity of 5-azacytidine and related nucleosides in C3H/10T 1/2 clone 8 and V79 cells [17].
  • C3H/10T 1/2 cells were treated with N-methyl-N'-nitro-N-nitrosoguanidine and then repeatedly exposed to formaldehyde (0.1 to 2.0 micrograms/ml) [18].
  • These studies also suggest that low concentrations of ascorbic acid in C3H/10T 1/2/CL8 cells can be effective in suppressing oncogenic progression only prior to a stage where an initiated cell achieves the capacity to grow in semisolid medium and to produce tumors in immunosuppressed animals [19].
  • Formaldehyde thus appears to be only a weak tumor promoter for C3H/10T 1/2 cell transformation [18].
  • Prostaglandin endoperoxide synthetase-dependent cooxidation of (+/-)-trans-7,8-dihydroxy-7,8-dihydrobenzo(a)pyrene in C3H/10T 1/2 clone 8 cells [20].

Regulatory relationships of 10T


Other interactions of 10T


Analytical, diagnostic and therapeutic context of 10T

  • We have examined the cooxidation of BP-7,8-diol in an intact cell culture system of C3H/10T 1/2 clone 8 mouse embryo fibroblasts, in which both the mixed-function oxidase and PES systems are present [20].
  • Southern blot analysis of VL30 DNA sequence organization in the DNA of two nontransformed mouse cell lines (AKR-2B, C3H/10T 1/2) and two chemically transformed derivatives (AKR-MCA, C3H/MCA-58) revealed 15 to 20 bands organized in an apparent strain-specific pattern [23].
  • Dose-rate effects in mammalian cells: V. Dose fractionation effects in noncycling C3H 10T 1/2 cells [24].
  • Now a rat PKC-beta1-overexpressing 10T 1/2 clone, PKC-4, with an 11-fold increase in PKC activity and an activated, partially transformed phenotype, links higher susceptibility to transformation through v-Ha-ras infection with an 80% increase in NAb binding assayed by flow cytometry [25].


  1. Antigenic similarity between cells transformed by ultraviolet radiation in vitro and in vivo. Fisher, M.S., Kripke, M.L., Chan, G.L. Science (1984) [Pubmed]
  2. Comparison of the malignant potential of 10T 1/2 cells and transformants with their survival responses to hyperthermia and to amphotericin B1. Hahn, G.M. Cancer Res. (1980) [Pubmed]
  3. Toxicity of firemaster FF-1 and 2,2',4,4',5,5'-hexabromobiphenyl in cultures of C3H/10T 1/2 mammalian fibroblasts. Bairstow, F., Hsia, M.T., Norback, D.H., Allen, J.R. Environ. Health Perspect. (1978) [Pubmed]
  4. Gene therapy: adenovirus-mediated human bone morphogenetic protein-2 gene transfer induces mesenchymal progenitor cell proliferation and differentiation in vitro and bone formation in vivo. Lou, J., Xu, F., Merkel, K., Manske, P. J. Orthop. Res. (1999) [Pubmed]
  5. Phagocytes as carcinogens: malignant transformation produced by human neutrophils. Weitzman, S.A., Weitberg, A.B., Clark, E.P., Stossel, T.P. Science (1985) [Pubmed]
  6. Removal of aflatoxin B1-DNA adducts and in vitro transformation in mouse embryo fibroblasts C3H/10T1 1/2. Amstad, P.A., Wang, T.V., Cerutti, P.A. J. Natl. Cancer Inst. (1983) [Pubmed]
  7. Embryonal carcinoma-derived growth factor activates protein kinase C in vivo and in vitro. Mahadevan, L.C., Aitken, A., Heath, J., Foulkes, J.G. EMBO J. (1987) [Pubmed]
  8. Loss of growth factor dependence and conversion of transforming growth factor-beta 1 inhibition to stimulation in metastatic H-ras-transformed murine fibroblasts. Schwarz, L.C., Gingras, M.C., Goldberg, G., Greenberg, A.H., Wright, J.A. Cancer Res. (1988) [Pubmed]
  9. Restoration of growth control in malignantly transformed mouse fibroblasts grown in a chemically defined medium. Tomei, L.D., Bertram, J.S. Cancer Res. (1978) [Pubmed]
  10. Partial down-regulation of protein kinase C in C3H 10T 1/2 mouse fibroblasts transfected with the human Ha-ras oncogene. Weyman, C.M., Taparowsky, E.J., Wolfson, M., Ashendel, C.L. Cancer Res. (1988) [Pubmed]
  11. Effect of formation and removal of aflatoxin B1:DNA adducts in 10T 1/2 mouse embryo fibroblasts on cell viability. Wang, T.C., Cerutti, P.A. Cancer Res. (1980) [Pubmed]
  12. Metabolic activation of benzo(a)pyrene by transformable and nontransformable C3H mouse fibroblasts in culture. Gehly, E.B., Heidelberger, C. Cancer Res. (1982) [Pubmed]
  13. Inhibition of induced differentiation of C3H/10T 1/2 clone 8 mouse embryo cells by tumor promoters. Mondal, S., Heidelberger, C. Cancer Res. (1980) [Pubmed]
  14. Out of balance: consequences of a partial keratin 10 knockout. Reichelt, J., Bauer, C., Porter, R., Lane, E., Magin, V. J. Cell. Sci. (1997) [Pubmed]
  15. Regulation of natural antibody binding and susceptibility to natural killer cells through Zn(++)-inducible ras oncogene expression. Tough, D.F., Haliotis, T., Chow, D.A. Int. J. Cancer (1992) [Pubmed]
  16. Congenic mice provide in vivo evidence for a genetic locus that modulates serum insulin-like growth factor-I and bone acquisition. Delahunty, K.M., Shultz, K.L., Gronowicz, G.A., Koczon-Jaremko, B., Adamo, M.L., Horton, L.G., Lorenzo, J., Donahue, L.R., Ackert-Bicknell, C., Kream, B.E., Beamer, W.G., Rosen, C.J. Endocrinology (2006) [Pubmed]
  17. Mutagenicity of 5-azacytidine and related nucleosides in C3H/10T 1/2 clone 8 and V79 cells. Landolph, J.R., Jones, P.A. Cancer Res. (1982) [Pubmed]
  18. Weak promotion of C3H/10T1/2 cell transformation by repeated treatments with formaldehyde. Frazelle, J.H., Abernethy, D.J., Boreiko, C.J. Cancer Res. (1983) [Pubmed]
  19. Differences in anchorage-dependent growth and tumorigenicities between transformed C3H/10T 1/2 cells with morphologies that are or are not reverted to a normal phenotype by ascorbic acid. Benedict, W.F., Wheatley, W.L., Jones, P.A. Cancer Res. (1982) [Pubmed]
  20. Prostaglandin endoperoxide synthetase-dependent cooxidation of (+/-)-trans-7,8-dihydroxy-7,8-dihydrobenzo(a)pyrene in C3H/10T 1/2 clone 8 cells. Boyd, J.A., Barrett, J.C., Eling, T.E. Cancer Res. (1982) [Pubmed]
  21. Neoplasms produced from C3H/10T 1/2 cells attached to plastic plates; saturation density, anchorage dependence and serum requirement of in vitro lines correlated with growth aggressiveness in vivo. Paranjpe, M., del Ande Eaton, S., Boone, C.W. J. Cell. Physiol. (1978) [Pubmed]
  22. Epidermal growth factor and tumor promoters prevent DNA fragmentation by different mechanisms. Kanter, P., Leister, K.J., Tomei, L.D., Wenner, P.A., Wenner, C.E. Biochem. Biophys. Res. Commun. (1984) [Pubmed]
  23. Organization and expression of endogenous virus-like (VL30) DNA sequences in nontransformed and chemically transformed mouse embryo cells in culture. Courtney, M.G., Schmidt, L.J., Getz, M.J. Cancer Res. (1982) [Pubmed]
  24. Dose-rate effects in mammalian cells: V. Dose fractionation effects in noncycling C3H 10T 1/2 cells. Zeman, E.M., Bedford, J.S. Int. J. Radiat. Oncol. Biol. Phys. (1984) [Pubmed]
  25. Protein kinase C expression links natural antibody binding with surveillance of activated and preneoplastic cells. Wang, H., Chow, D.A. Scand. J. Immunol. (1999) [Pubmed]
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