A tumor suppressor gene, Cx26, also mediates the bystander effect in HeLa cells

Cancer Research

Volumn 57, Issue 14, 1997, Pages 2929-2932

  Mesnil, Marc ^a   Piccoli, Colette ^a   Yamasaki, Hiroshi ^a  

^a INTERNATIONAL AGENCY FOR RESEARCH ON CANCER   (France)

Author keywords

[No Author keywords available]

Indexed keywords

18ALPHA GLYCYRRHETINIC ACID; GANCICLOVIR; THYMIDINE KINASE;

ARTICLE; CANCER INHIBITION; CELL COMMUNICATION; CELL JUNCTION; CELL KILLING; DRUG TOXICITY; GENE THERAPY; HELA CELL; HUMAN; HUMAN CELL; PRIORITY JOURNAL; TUMOR SUPPRESSOR GENE;

CONNEXINS; GANCICLOVIR; GENES, TUMOR SUPPRESSOR; HELA CELLS; HUMANS; THYMIDINE KINASE;

EID: 0030750649     PISSN: 00085472     EISSN: None     Source Type: Journal    
DOI: None     Document Type: Article

References (19)

1. Freeman, S. M., Abboud, C. N., Whartenby, K. A., Packman, C. H., Koeplin, D. S., Moolten, F. L., and Abraham, G. N. The "bystander effect": tumor regression when a fraction of the tumor mass is genetically modified. Cancer Res., 53: 5274-5283, 1993.
2. Ram, Z., Culver, K. W., Walbridge, S., Blaese, R. M., and Oldfield, E. H. In situ retroviral-mediated gene transfer for the treatment of brain tumors in rats. Cancer Res., 53: 83-88, 1993.
3. Yamasaki, H., and Katoh, F. Novel method for selective killing of transformed rodent cells through intercellular communication with possible therapeutic application. Cancer Res., 48: 3203-3207, 1988.
4. Mesnil, M., Piccoli, C., Tiraby, G., Willecke, K., and Yamasaki, H. Bystander killing of cancer cells by herpes simplex virus thymidine kinase gene is mediated by connexins. Proc. Natl. Acad. Sci. USA, 93: 1831-1835, 1996.
5. Bi, W. L., Parysek, L. M., Warnick, R., and Stambrook, P. J. In vitro evidence that metabolic cooperation is responsible for the bystander effect observed with HSV-tk retroviral gene therapy. Hum. Gene Ther., 4: 725-731, 1993.
6. Fick, J., Barker, F. G., II, Dazin, P., Westphale, E. M., Beyer, E. C., and Israel, M. A. The extent of heterocellular communication mediated by gap junctions is predictive of bystander tumor cytotoxicity in vitro. Proc. Natl. Acad. Sci. USA, 92: 11071-11075, 1995.
7. Elshami, A. A., Saavedra, A., Zhang, H., Kucharczuk, J. C., Spray, D. C., Fishman, G. I., Amin, K. M., Kaiser, L. R., and Albelda, S. M. Gap junctions play a role in the "bystander effect" of the herpes simplex virus thymidine kinase/canciclovir system in vitro. Gene Ther., 3: 83-92, 1996.
8. Mesnil, M., Oyamada, M., Fitzgerald, D. J., Jongen, W. M. F., Krutovskikh, V., and Yamasaki, H. Gap junctional communication alterations at various regulatory levels of connexin expression and function during animal and human carcinogenesis. Prog. Cell Res., 3: 311-316, 1993.
9. Sacco, M. G., Benedetti, S., Duflot-Dancer, A., Mesnil, M., Bagnasco, L., Strina, D., Fasolo, V., Villa, A., Macchi, P., Faranda, S., Vozzoni, P., and Finocchiaro, G. Partial regression, yet incomplete eradication or mammary tumors in transgenic mice by retrovirally mediated HSV-tk transfer "in vitro." Gene Ther., 3: 1151-1156, 1996.
10. Yamasaki, H., and Naus, C. C. G. Role of connexin genes in growth control. Carcinogenesis (Lond.), 17: 1199-1213, 1996.
11. Eghbali, B., Kessler, J. A., Reid, L. M., Roy, C., and Spray, D. C. Involvement of gap junctions in tumorigenesis: transfection of tumor cells with connexin 32 cDNA retards growth in vivo. Proc. Natl. Acad. Sci. USA, 88: 10701-10705, 1991.
12. Zhu, D., Caveney, S., Kidder, G. M., and Naus, C. C. G. Transfection of C6 glioma cells with connexin 43 cDNA: analysis of expression, intercellular coupling, and cell proliferation. Proc. Natl. Acad. Sci. USA, 88: 1883-1887, 1991.
13. Rose, B., Mehta, P. P., and Loewenstein, W. R. Gap-junction protein gene suppresses tumorigenicity. Carcinogenesis (Lond.), 14: 1073-1075, 1993.
14. Naus, C. C. G., Elisevich, K., Zhu, D., Belliveau, D. J., and Del Maestro, R. F. In vivo growth of C6 glioma cells transfected with connexin 43 cDNA. Cancer Res., 52: 4208-4213, 1992.
15. Mesnil, M., Krutovskikh, V., Piccoli, C., Elfgang, C., Traub, O., Willecke, K., and Yamasaki, H. Negative growth control of HeLa cells by connexin genes: connexin species specificity. Cancer Res., 55: 629-639, 1995.
16. Elfgang, C., Eckert, R., Lichtenberg-Fraté, H., Butterweck, A., Traub, O., Klein, R. A., Hülser, D. F., and Willecke, K. Specific permeability and selective formation of gap junction channels in connexin-transfected HeLa cells. J. Cell Biol., 129: 805-817, 1995.
17. Davidson, J. S., Baumgarten, I. M., and Harley, B. H. Reversible inhibition of intercellular junctional communication by glycyrrhetinic acid. Biochem. Biophys. Res. Commun., 134: 29-36, 1986.
18. Hirschi, K. K., Xu, C-E., Tsukamoto, T., and Sager, R. Gap junction genes Cx26 and Cx43 individually suppress the cancer phenotype of human mammary carcinoma cells and restore differentiation potential. Cell Growth & Differ., 7: 861-870, 1996.
19. Mesnil, M., Asamoto, M., Piccoli, C., and Yamasaki, H. Possible molecular mechanism of homologous and heterologous gap junctional intercellular communication in rat liver epithelial cell lines. Cell Adhesion Commun., 2: 377-384, 1994.