JB6 Highlights 2001 and References
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The mouse Balb/C JB6 model (1) is the only well characterized model
of genetic variants for a neoplastic transformation response to tumor promoters.
These cells are not differentially sensitive to tumor promoter induced
mitogenesis or differentiation (2), thus increasing the likelihood that
molecular response differences will be transformation-relevant. These
cells are also not differential at the level of tumor promoter receptors
such as protein kinase C or epidermal growth factor receptor, thus indicating
that these are post-receptor signaling variants (3). Moreover the
JB6 response variants are stably free of spontaneous transformation (a
property found to be mouse strain dependent) and stably responsive (P+)
or nonresponsive (P-) to tumor promoter induced transformation. Thus
molecular events that occur only in the P+ cells are candidates for mediating
tumor promotion while those that occur only in the P- cells are candidate
inhibitors. The JB6 model is not suitable for studying epidermal
differentiation or keratin synthesis. The JB6 model is uniquely suited
for studying tumor promotion and promotion-relevant molecular events.
Research using the Balb/C mouse JB6 model of transformation response variants
has yielded milestones that propelled research in several areas.
Mechanistic Insights
The JB6 model was among the first (along with those reported by M.
Oren and his colleagues (4) in which expression of a mutant of the tumor
suppressor p53 was shown to produce a gain of oncogenic response (5).
The first cloning of mouse TIMP-3 was done as part of a differential display
analysis of JB6 cells (6). The demonstration that TIMP-3 functions as a
tumor suppressor in human colon carcinoma cells (7) was supported by others
who isolated TIMP-3 by gene trapping (8). The first observation of
a requirement for active oxygen generation in tumor promotion was made
with JB6 cells (9) and has been followed up extensively (10-15).
The ubiquitous secreted cell adhesion glycophosphoprotein osteopontin was
first cloned in 1987 from JB6 cells by subtractive hybridization (16).
Osteopontin expression plays important roles in tumor promotion and tumor
progression, inflammation, bone remodeling and other processes (17-19).
The 1989 discovery (20) and subsequent reports (21, 22) that the JB6 transformation
variants are also AP-1 response variants stimulated the demonstration that
AP-1 activation is causal for progression/ invasion (23, 24), maintenance
(25), and induction (26) of tumor phenotype in mouse cell culture models.
These findings stimulated in vivo investigations that implicated cFos in
papilloma-to- carcinoma progression but not in tumor promotion (papilloma
induction) (27). That tumor promotion in vivo requires AP-1 activation
was first established using dominant negative jun(TAM67) expressing transgenic
mice (28). Transformation relevant pathways to AP-1 activation
have been elucidated in JB6 cells, implicating MAP kinase ERK activation
(29, 30). The ERK requirement for AP-1 activation has been extended
to AP-1 activation by UVB (31) and by arsenite (32). The observation
that UVB activates AP-1 has been extended from JB6 cells to human keratinocytes
(33, 34) and to mouse skin in vivo (35, 36). NF B-dependent gene
expression is also required for transformation in the JB6 model (14).
P- cells are nonresponsive for NF B activation (14). Inducible nitric
oxide synthase (iNOS) is induced in P+ but not in P- JB6 cells cocultured
with an interferon- -stimulated macrophage cell line (37). INOS induction
is NF B-dependent. iNOS is one of a small set of genes that appears
to be targeted in mice expressing AP-1/NF B inhibitor (TAM67) (Young et
al., unpublished).
Cancer Prevention
In addition to propelling mechanistic insights, studies with the JB6
model have impacted research in cancer prevention. A number of tumor
promotion inhibitors studied in the JB6 model have been discovered to owe
their transformation inhibiting activity at least in part to their AP-1
repressing activity. Among these inhibitors are turmeric-derived curcumin
(38), aspirin (39), the tea polyphenol EGCG (40-42), potato proteinase
inhibitors (43, 44), gingerol (45), citrifolin A (46), Omega 3 fatty acids
(47), and novel glycosides (48). Some of these inhibitors have
been shown to target AP-1 also in mouse skin (35). Recently Birt and colleagues
have discovered that the basis for caloric restriction inhibiting tumor
promotion lies at least in part, in its inhibition of ERK and AP-1 activation
(49, 50). Other molecular targets of cancer prevention agents have
been identified using the JB6 model. The grape skin inhibitor resveratrol
activates p53 (51).
Cancer Risk Assessment
Finally, the JB6 model has also been valuable for cancer risk assessment.
The sensitivity of the JB6 model has made it possible to convincingly conclude
that exposure to electric and magnetic fields around power lines poses
little or no human risk (52, 53). Environmental metals such as arsenic
and vanadium have been shown to act as tumor promoters in the JB6 model
(32, 54).
In summary the use of the mouse JB6 model has spawned a number of advances
not only in basic cell biology but also in understanding the molecular
mechanism of tumor promotion. Moreover these studies have contributed
to progress in cancer prevention and risk assessment research. Many
of these advances have been extended from the JB6 model to human epithelial
cell (solid tumor) progression models or to in vivo mouse multistage carcinogenesis
models. This progress reflects a response of many laboratories to
the unique opportunities for discovery presented by the mouse JB6 model.
References:
1. Colburn N. H., Former B. F., Nelson K. A., Yuspa
S. H.: Tumour promoter induces anchorage independence irreversibly. Nature
281: 589-591, 1979.
2. Colburn N. H., Wendel E. J., Abruzzo G.: Dissociation
of mitogenesis and late-stage promotion of tumor cell phenotype by phorbol
esters: mitogen-resistant variants are sensitive to promotion. Proc Natl
Acad Sci U S A 78: 6912-6916, 1981.
3. Colburn N. H., Gindhart T. D., Hegamyer G. A.,
Blumberg P. M., Delclos K. B., Magun B. E., Lockyer J.: Phorbol diester
and epidermal growth factor receptors in 12-O- tetradecanoylphorbol-13-acetate-resistant
and -sensitive mouse epidermal cells. Cancer Res 42: 3093-3097, 1982.
4. Shaulian E., Zauberman A., Ginsberg D., Oren
M.: Identification of a minimal transforming domain of p53: negative dominance
through abrogation of sequence- specific DNA binding. Mol Cell Biol 12:
5581-5592, 1992.
5. Sun Y., Nakamura K., Wendel E., Colburn N.:
Progression toward tumor cell phenotype is enhanced by overexpression of
a mutant p53 tumor-suppressor gene isolated from nasopharyngeal carcinoma.
Proc Natl Acad Sci U S A 90: 2827-2831, 1993.
6. Sun Y., Hegamyer G., Colburn N. H.: Molecular
cloning of five messenger RNAs differentially expressed in preneoplastic
or neoplastic JB6 mouse epidermal cells: one is homologous to human tissue
inhibitor of metalloproteinases-3. Cancer Res 54: 1139-1144, 1994.
7. Bian J., Wang Y., Smith M. R., Kim H., Jacobs
C., Jackman J., Kung H. F., Colburn N. H., Sun Y.: Suppression of in vivo
tumor growth and induction of suspension cell death by tissue inhibitor
of metalloproteinases (TIMP)-3. Carcinogenesis 17: 1805- 1811, 1996.
8. Andreu T., Beckers T., Thoenes E., Hilgard P.,
von Melchner H.: Gene trapping identifies inhibitors of oncogenic transformation.
The tissue inhibitor of metalloproteinases-3 (TIMP3) and collagen type
I alpha2 (COL1A2) are epidermal growth factor-regulated growth repressors.
J Biol Chem 273: 13848-13854, 1998.
9. Nakamura Y., Colburn N. H., Gindhart T. D.:
Role of reactive oxygen in tumor promotion: implication of superoxide anion
in promotion of neoplastic transformation in JB-6 cells by TPA. Carcinogenesis
6: 229-235, 1985.
10. Crawford D., Zbinden I., Amstad P., Cerutti
P.: Oxidant stress induces the protooncogenes c-fos and c-myc in mouse
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11. Ghosh R., Amstad P., Cerutti P.: UVB-induced
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Berezesky I. K., Trump B. F.: bcl-2 enhancement of malignant transformation
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13. Gupta A., Rosenberger S. F., Bowden G. T.:
Increased ROS levels contribute to elevated transcription factor and MAP
kinase activities in malignantly progressed mouse keratinocyte cell lines.
Carcinogenesis 20: 2063-2073, 1999.
14. Hsu T.-C., Nair R., Tulsian P., Hegamyer G.,
Young M. R., Colburn N. H.: Transformation non-responsive cells owe their
resistance to lack of NF- B activation. Cancer Res 61: 4160-4168, 2001.
15. Hsu T. C., Young M. R., Cmarik J., Colburn
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16. Craig A. M., Smith J. H., Denhardt D. T.: Osteopontin,
a transformation-associated cell adhesion phosphoprotein, is induced by
12-O-tetradecanoylphorbol 13-acetate in mouse epidermis. J Biol Chem 264:
9682-9689, 1989.
17. Denhardt D. T., Giachelli C. M., Rittling S.
R.: Role of osteopontin in cellular signaling and toxicant injury. Annu
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18. Chang P. L., Prince C. W.: 1 alpha,25-dihydroxyvitamin
D3 stimulates synthesis and secretion of nonphosphorylated osteopontin
(secreted phosphoprotein 1) in mouse JB6 epidermal cells. Cancer Res 51:
2144-2150, 1991.
19. Chang P. L., Chambers A. F.: Transforming JB6
cells exhibit enhanced integrin- mediated adhesion to osteopontin. J Cell
Biochem 78: 8-23, 2000.
20. Bernstein L. R., Colburn N. H.: AP1/jun function
is differentially induced in promotion-sensitive and resistant JB6 cells.
Science 244: 566-569, 1989.
21. Ben-Ari E. T., Bernstein L. R., Colburn N.
H.: Differential c-jun expression in response to tumor promoters in JB6
cells sensitive or resistant to neoplastic transformation. Mol Carcinog
5: 62-74, 1992.
22. Bernstein L. R., Bravo R., Colburn N. H.: 12-O-tetradecanoylphorbol-13-acetate--
induced levels of AP-1 proteins: a 46-kDa protein immunoprecipitated by
anti-fra-1 and induced in promotion-resistant but not promotion-sensitive
JB6 cells. Mol Carcinog 6: 221-229, 1992.
23. Hennigan R. F., Hawker K. L., Ozanne B. W.:
Fos-transformation activates genes associated with invasion. Oncogene 9:
3591-3600, 1994.
24. Lamb R. F., Hennigan R. F., Turnbull K., Katsanakis
K. D., MacKenzie E. D., Birnie G. D., Ozanne B. W.: AP-1-mediated invasion
requires increased expression of the hyaluronan receptor CD44. Mol Cell
Biol 17: 963-976, 1997.
25. Domann F. E., Levy J. P., Birrer M. J., Bowden
G. T.: Stable expression of a c-JUN deletion mutant in two malignant mouse
epidermal cell lines blocks tumor formation in nude mice. Cell Growth Differ
5: 9-16, 1994.
26. Dong Z., Birrer M. J., Watts R. G., Matrisian
L. M., Colburn N. H.: Blocking of tumor promoter-induced AP-1 activity
inhibits induced transformation in JB6 mouse epidermal cells. Proc Natl
Acad Sci U S A 91: 609-613, 1994.
27. Saez E., Rutberg S. E., Mueller E., Oppenheim
H., Smoluk J., Yuspa S. H., Spiegelman B. M.: c-fos is required for malignant
progression of skin tumors. Cell 82: 721-732, 1995.
28. Young M. R., Li J. J., Rincon M., Flavell R.
A., Sathyanarayana B. K., Hunziker R., Colburn N.: Transgenic mice demonstrate
AP-1 (activator protein-1) transactivation is required for tumor promotion.
Proc Natl Acad Sci U S A 96: 9827-9832, 1999.
29. Watts R. G., Huang C., Young M. R., Li J. J.,
Dong Z., Pennie W. D., Colburn N. H.: Expression of dominant negative Erk2
inhibits AP-1 transactivation and neoplastic transformation. Oncogene 17:
3493-3498, 1998.
30. Huang C., Ma W. Y., Young M. R., Colburn N.,
Dong Z.: Shortage of mitogen- activated protein kinase is responsible for
resistance to AP-1 transactivation and transformation in mouse JB6 cells.
Proc Natl Acad Sci U S A 95: 156-161, 1998.
31. Huang C., Ma W. Y., Dong Z.: The extracellular-signal-regulated
protein kinases (Erks) are required for UV-induced AP-1 activation in JB6
cells. Oncogene 18: 2828- 2835, 1999.
32. Huang C., Ma W. Y., Li J., Goranson A., Dong
Z.: Requirement of Erk, but not JNK, for arsenite-induced cell transformation.
J Biol Chem 274: 14595-14601, 1999.
33. Chen W., Borchers A. H., Dong Z., Powell M.
B., Bowden G. T.: UVB irradiation- induced activator protein-1 activation
correlates with increased c-fos gene expression in a human keratinocyte
cell line. J Biol Chem 273: 32176-32181, 1998.
34. Barthelman M., Bair W. B., 3rd, Stickland K.
K., Chen W., Timmermann B. N., Valcic S., Dong Z., Bowden G. T.: (-)-Epigallocatechin-3-gallate
inhibition of ultraviolet B-induced AP-1 activity. Carcinogenesis 19: 2201-2204,
1998.
35. Huang C., Ma W. Y., Hanenberger D., Cleary
M. P., Bowden G. T., Dong Z.: Inhibition of ultraviolet B-induced activator
protein-1 (AP-1) activity by aspirin in AP-1-luciferase transgenic mice.
J Biol Chem 272: 26325-26331, 1997.
36. Barthelman M., Chen W., Gensler H. L., Huang
C., Dong Z., Bowden G. T.: Inhibitory effects of perillyl alcohol on UVB-induced
murine skin cancer and AP-1 transactivation. Cancer Res 58: 711-716, 1998.
37. Murakami A., Kawabata K., Koshiba T., Gao G.,
Nakamura Y., Koshimizu K., Ohigashi H.: Nitric oxide synthase is induced
in tumor promoter-sensitive, but not tumor promoter-resistant, JB6 mouse
epidermal cells cocultured with interferon- gamma-stimulated RAW 264.7
cells: the role of tumor necrosis factor-alpha. Cancer Res 60: 6326-6331,
2000.
38. Lu Y. P., Chang R. L., Lou Y. R., Huang M.
T., Newmark H. L., Reuhl K. R., Conney A. H.: Effect of curcumin on 12-O-tetradecanoylphorbol-13-acetate-
and ultraviolet B light-induced expression of c-Jun and c-Fos in JB6 cells
and in mouse epidermis. Carcinogenesis 15: 2363-2370, 1994.
39. Dong Z., Huang C., Brown R. E., Ma W. Y.: Inhibition
of activator protein 1 activity and neoplastic transformation by aspirin.
J Biol Chem 272: 9962-9970, 1997.
40. Dong Z., Ma W., Huang C., Yang C. S.: Inhibition
of tumor promoter-induced activator protein 1 activation and cell transformation
by tea polyphenols, (-)- epigallocatechin gallate, and theaflavins. Cancer
Res 57: 4414-4419, 1997.
41. Nomura M., Ma W. Y., Huang C., Yang C. S.,
Bowden G. T., Miyamoto K., Dong Z.: Inhibition of ultraviolet B-induced
AP-1 activation by theaflavins from black tea. Mol Carcinog 28: 148-155,
2000.
42. Nomura M., Ma W., Chen N., Bode A. M., Dong
Z.: Inhibition of 12-O- tetradecanoylphorbol-13-acetate-induced NF-kappaB
activation by tea polyphenols, (-)-epigallocatechin gallate and theaflavins.
Carcinogenesis 21: 1885-1890, 2000.
43. Huang C., Ma W. Y., Ryan C. A., Dong Z.: Proteinase
inhibitors I and II from potatoes specifically block UV- induced activator
protein-1 activation through a pathway that is independent of extracellular
signal-regulated kinases, c-Jun N-terminal kinases, and P38 kinase. Proc
Natl Acad Sci U S A 94: 11957-11962, 1997.
44. Liu G., Chen N., Kaji A., Bode A. M., Ryan
C. A., Dong Z.: Proteinase inhibitors I and II from potatoes block UVB-induced
AP-1 activity by regulating the AP-1 protein compositional patterns in
JB6 cells. Proc Natl Acad Sci U S A 98: 5786-5791, 2001.
45. Bode A. M., Ma W. Y., Surh Y. J., Dong Z.:
Inhibition of epidermal growth factor- induced cell transformation and
activator protein 1 activation by. Cancer Res 61: 850- 853, 2001.
46. Sang S., He K., Liu G., Zhu N., Cheng X., Wang
M., Zheng Q., Dong Z., Ghai G., Rosen R. T., Ho C. T.: A new unusual iridoid
with inhibition of activator protein-1 (AP-1) from the leaves of Morinda
citrifolia L. Org Lett 3: 1307-1309, 2001.
47. Liu G., Bibus D. M., Bode A. M., Ma W. Y.,
Holman R. T., Dong Z.: Omega 3 but not omega 6 fatty acids inhibit AP-1
activity and cell transformation in JB6 cells. Proc Natl Acad Sci U S A
98: 7510-7515, 2001.
48. Liu G., Bode A., Ma W. Y., Sang S., Ho C. T.,
Dong Z.: Two novel glycosides from the fruits of morinda citrifolia (noni)
inhibit ap-1 transactivation and cell transformation in the mouse epidermal
jb6 cell line. Cancer Res 61: 5749-5756, 2001.
49. Liu Y., Duysen E., Yaktine A. L., Au A., Wang
W., Birt D. F.: Dietary energy restriction inhibits ERK but not JNK or
p38 activity in the epidermis of SENCAR mice. Carcinogenesis 22: 607-612,
2001.
50. Birt D. F., Yaktine A., Duysen E.: Glucocorticoid
mediation of dietary energy restriction inhibition of mouse skin carcinogenesis.
J Nutr 129: 571S-574S, 1999.
51. She Q. B., Bode A. M., Ma W. Y., Chen N. Y.,
Dong Z.: Resveratrol-induced activation of p53 and apoptosis is mediated
by extracellular-signal-regulated protein kinases and p38 kinase. Cancer
Res 61: 1604-10., 2001.
52. Saffer J. D., Chen G., Colburn N. H., Thurston
S. J.: Power frequency magnetic fields do not contribute to transformation
of JB6 cells. Carcinogenesis 18: 1365-1370, 1997.
53. West R. W., Hinson W. G., Swicord M. L.: Anchorage-independent
growth with JB6 cells exposed to 60 HZ magnetic fields at several flux
densities. Bioelectrochemistry & Bioenergetics 39: 175-179, 1996.
54. Ding M., Li, J.-J., Leonard, S.S., Ye, J.-P.,
Shi, X., Colburn, N.H., Castranova, V. andVallyathan, V.: Vanadate-induced
activation
of activator protein-1: Role of reactiveoxygen species. Carcinogenesis
20: 663-668, 1999.
JB6 Bibliography (1978-date)
1978
-
Colburn, N.H., Vorder Bruegge, W.F., Bates, J.R., Gray, R.H.,
Rossen, J.D., Kelsey, W.H., and Shimada, T. Correlation of anchorage
independent growth with tumorigenicity of chemically transformed mouse
epidermal cells. Cancer Res. 38: 624-634, 1978.
-
Colburn, N.H. Chemical transformation of epidermal
cell cultures. In Saffiotti, U. and Autrup, H. (Eds.): In Vitro
Carcinogenesis. National Cancer Institute. Technical Report
Series 44, 1978, pp. 69-94.
-
Colburn, N.H., Vorder Bruegge, W.F., Bates, J., and Yuspa,
S.H. Epidermal cell transformation in vitro. In Slaga, T.J.,
Sivak, A., and Boutwell, R.K. (Eds.): Mechanisms of Tumor Promotion
and Cocarcinogenesis. New York, Raven Press, 1978, pp. 257-271.
1979
-
Colburn, N.H., Former, B.F., Nelson K.A., and Yuspa, S.H.
Tumor promoter induces anchorage independence irreversibly. Nature
281: 589-591, 1979.
-
Colburn N.H. The use of tumor promoter responsive epidermal
cell lines to study preneoplastic progression. In Franks, L.M. and
Wigley, C.B. (Eds.): Neoplastic Transformation in Differentiated
Epithelial Cell Systems in vitro. New York, Academic Press, 1979,
pp. 113-134.
1980
-
Colburn, N.H. Tumor promotion and preneoplastic progression.
In Slaga, T.J. (Ed.): Carcinogenesis; Modifiers of Carcinogenesis,
Vol. 5. New York, Raven Press, 1980, pp. 33-56.
-
Colburn, N.H., Koehler, B., and Nelson, K.A. A cell
culture assay for tumor promoter dependent progression toward neoplastic
phenotype: detection of tumor promoters and promotion inhibitors.
Teratogenesis, Carcinog. Mutagen. 1: 87-96, 1980.
-
Colburn, N.H. Tumor promoter produces anchorage independence
in mouse epidermal cells by an induction mechanism. Carcinogenesis
1: 951-954, 1980.
1981
-
Colburn, N.H. and Gindhart, T. Specific binding of
transforming growth factor correlates with promotion of anchorage independence
in EGF receptorless JB6 cells. Biochem. Biophys. Res. Commun. 102:
799-807, 1981.
-
Colburn, N.H., Wendel, E., and Abruzzo, G. Dissociation
of mitogenesis and late-stage promotion of tumor cell phenotype by phorbol
esters: mitogen resistant variants are sensitive to promotion.
Proc. Natl. Acad. Sci. USA 78: 6912-6916, 1981.
-
Dion, L.D., DeLuca, L., and Colburn, N.H. Phorbol ester-induced
anchorage independence and its antagonism by retinoic acid correlates with
altered expression of specific glycoproteins. Carcinogenesis 2:
951-958, 1981.
1982
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Colburn, N.H., Dion, L.D., and Wendel, E.J. The role
of mitogenic stimulation and specific glycoprotein changes in the mechanism
of late-stage promotion in JB-6 epidermal cell lines. In Hecker,
E., Fusening, N. E., Kunz, W., Marks, F., and Thielmann, H.W. (Eds.):
Carcinogenesis: A Comprehensive Survey. New York, Raven Press, 1982,
pp. 231-235.
-
Colburn, N. and Huberman, E. Tumor promotion:
workshop report. In Haris, C.C. and Cerutti, P.A. (Eds.): Mechanisms
of Chemical Carcinogenesis. New York, Alan R. Liss, 1982, pp. 499-501.
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Colburn, N.H., Wendel, E. and Srinivas, L. Responses
of preneoplastic epidermal cells to tumor promoters and growth factors:
use of promoter resistant variants for mechanism studies. J. Cell.
Biochem. 18: 261-270, 1982.
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Srinivas, L. and Colburn, N.H. Tumor promoter induced
ganglioside changes in promotable mouse epidermal cells: antagonism
by an antipromoter. J. Natl. Cancer Inst. 68: 469-473, 1982.
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Colburn, N.H., Gindhart, T., Hegamyer, G., Blumberg, P.M.,
Delclos, K.B., Magun, B.E., and Lockyer, L. Phorbol diester and EGF
receptors in TPA-resistant and TPA-sensitive mouse epidermal cells.
Cancer Res. 42: 3093-3097, 1982.
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Srinivas, L., Gindhart, T.D., and Colburn, N.H. TPA
resistant cells lack trisialoganglioside (GT) response. Proc. Natl.
Acad. Sci. USA 79: 4988-4991, 1982.
-
Dion, L.D., Bear, J., Bateman, J., Deluca, L.M., and Colburn,
N.H. Tumor promoting phorbol ester inhibits procollagen synthesis
in promotable JB6 mouse epidermal cells. J. Natl. Cancer Inst. 69:
1147-1154, 1982.
1983
-
Bondy G. P., Denhardt D. T.: Exposure of JB6 mouse epidermal
cells to 12-0-tetradecanoyl- phorbol-13-acetate is not accompanied by a
significant change in total DNA-cytosine methylation. Carcinogenesis 4:
1599-1603, 1983.
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Colburn, N.H., Talmadge, C.B., and Gindhart, T.D. Transfer
of sensitivity to tumor promoters by transfection of DNA from sensitive
into insensitive mouse JB6 epidermal cells. Mol. Cell. Biol. 3:
1182-1186, 1983.
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Colburn, N.H., Gindhart, T.D., Dalal, B., and Hegamyer, G.A.
The role of phorbol ester receptor binding in responses to promoters by
mouse and human cells. In Langenbach, R., Nesnow, S., and Rice, J.
(Eds.): Organ and Species Specificity in Chemical Carcinogenesis.
New York, Plenum Publishing Corp., 1983, pp. 189-200.
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Colburn, N.H., Talmadge, C.B., and Gindhart, T.D. Transfer
of phorbol ester promotability by transfection of DNA from promotable into
nonpromotable cells. In Cohn W.E. (Ed.): Progress in Nucleic
Acid Research and Molecular Biology. New York, Academic Press, 1983,
pp. 107-110.
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Copley, M., Gindhart, T., and Colburn, N. Hexose uptake
as an indicator of JB6 mouse epidermal cell resistance to the mitogenic
activity of TPA. J. Cell. Physiol. 114: 173-178, 1983.
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Gensler H. L., Bowden G. T.: Evidence suggesting a dissociation
of DNA strand scissions and late- stage promotion of tumor cell phenotype.
Carcinogenesis 4: 1507-1511, 1983.
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Sobel, M.E., Dion, L.D., Vuust, Jens, and Colburn, N.H.
Tumor promoting phorbol esters inhibit procollagen synthesis at a pretranslational
level in JB6 mouse epidermal cells. Mol. Cell. Biol. 3: 1527-1532,
1983.
1984
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Srinivas, L. and Colburn, N.H. Preferential oxidation
of cell surface sialic acid by periodate leads to promotion of transformation
in JB6 cells. Carcinogenesis 5: 515-519, 1984.
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Srinivas, L. and Colburn, N.H. Reduced trisialoganglioside
synthesis in chemically but not mos-transformed mouse epidermal cells.
Cancer Res. 44: 1510-1514, 1984.
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Colburn, N.H., Lerman, M.I., Srinivas, L., Nakamura, Y.,
Hegamyer, G.A., and Gindhart, T.D. Membrane and genetic events in
tumor promotion: studies with promoter resistant variants of JB6
cells. In Fujiki, H. (Ed.): Cellular Interactions by Environmental
Tumor Promoters. Tokyo, Japan Sci. Soc. Press, 1984, pp. 155-166.
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Colburn, N.H., Lerman, M.I., Srinivas, L., Nakamura, Y.,
Hegamyer, G.A., and Gindhart, T.D. Genetic determinants of tumor
promotion: studies with promoter resistant variants of JB6 cells.
In Bishop, M., Graves, M., and Rowley, T. (Eds.): Genes and Cancer,
Vol. 17. New York, Alan R. Liss, 1984, pp. 137-155.
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Colburn, N.H., Srinivas, L., Hegamyer, G.A., Dion, L.D.,
and Wendel, E.J. Role of specific membrane and genetic changes in
the mechanism of tumor promotion. Studies with promoter-resistant
variants. In Borsonyi, M. (Ed.): The Role of CoCarcinogens
and Promoters in Human and Experimental Carcinogenesis. Lyon, France,
IARC Publication, 1984, pp. 205-215.
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Feuerstein N., Sahai A., Anderson W. B., Salomon D., Cooper
H. L.: Differential phosphorylation events associated with phorbol ester
effects on acceleration versus inhibition of cell growth. Cancer Res 44:
5227-5233, 1984.
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Fleischmann, W.R., Jr., Newton, R.C., Fleischmann, C.M.,
Colburn, N.H., and Brysk, M.M. Discrimination between nonmalignant
and malignant cells by combinations of IFN- plus IFN- /ß.
J. Bio. Response Mod. 3: 397-405, 1984.
-
Gindhart T. D., Stevens L., Copley M. P.: Transformation
and tumor promoter sensitive phosphoproteins in JB6 mouse epidermal cells:
one is also sensitive to heat stress. Carcinogenesis 5: 1115-1121, 1984.
1985
-
Colburn, N.H., Lerman, M.I., Hegamyer, G.A., and Gindhart,
T.D. A transforming activity not detectable by DNA transfection to
NIH 3T3 cells is detected by JB6 mouse epidermal cells. Mol. Cell.
Biol. 5: 890-893, 1985.
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Colburn, N.H. Genes and membrane signals involved in
neoplastic transformation. In Huberman, E. and Barr, S. H. (Eds.):
Carcinogenesis: A Comprehensive Survey. The Role of Chemicals and
Radiation in the Etiology of Cancer. New York, Raven Press, 1985,
Vol. 10, pp. 235-248.
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Huang C., Bode A. M., Chen N. Y., Ma W. Y., Li J., Nomura
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mice by arsenite and arsenate. Anticancer Res 21: 261-7, 2001.
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Huang, C., Li, J., Ding, M., Leonard, S.S., Wang, L., Castranova,
V., Vallyathan, V., and Shi, X. UV induces phosphorylation of protein
kinase B (Akt) at Ser-473 and Thr-308 in mouse epidermal Cl 41 cells through
hydrogen peroxide. J. Biol. Chem. 276: 40234-40240, 2001.
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Kumar NV, Bernstein LR. Ten ERK-related proteins in
three distinct classes associate with AP-1 proteins and/or AP-1 DNA.
J Biol Chem. 2001 Aug 24;276(34):32362-72.
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Liu G., Bode A., Ma W. Y., Sang S., Ho C. T., Dong Z.: Two
novel glycosides from the fruits of Morinda citrifolia (noni) inhibit AP-1
transactivation and cell transformation in the mouse epidermal JB6 cell
line. Cancer Res 61: 5749-56, 2001.
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Liu G., Chen N., Kaji A., Bode A. M., Ryan C. A., Dong Z.:
Proteinase inhibitors I and II from potatoes block UVB-induced AP-1 activity
by regulating the AP-1 protein compositional patterns in JB6 cells. Proc
Natl Acad Sci U S A 98: 5786-91, 2001.
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Nomura M., Kaji A., Ma W. Y., Zhong S., Liu G., Bowden G.
T., Miyamoto K., Dong Z.: Mitogen- and stress-activated protein kinase
1 mediates activation of akt by ultraviolet b irradiation. J Biol Chem
276: 25558-67, 2001.
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Nomura M., Kaji A., Ma W., Miyamoto K., Dong Z.: Suppression
of cell transformation and induction of apoptosis by caffeic acid phenethyl
ester. Mol Carcinog 31: 83-9, 2001.
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Nomura, M., Kaji, A., He, Z., Ma, W-Y., M, K-i., Yang, C.S.,
and Dong, Z. Inhibitory mechanisms of tea polyphenols on the ultraviolet
B-activated phosphatidylinositol 3-kinase-dependent pathway. J. Biol.
Chem. 276: 46624-46631, 2001.
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Pisha E., Lui X., Constantinou A. I., Bolton J. L.: Evidence
that a metabolite of equine estrogens, 4-hydroxyequilenin, induces cellular
transformation in vitro. Chem Res Toxicol 14: 82- 90, 2001.
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Przybyszewski J., Yaktine A. L., Duysen E., Blackwood D.,
Wang W., Au A., Birt D. F.: Inhibition of phorbol ester-induced AP-1-DNA
binding, c-Jun protein and c-jun mRNA by dietary energy restriction is
reversed by adrenalectomy in SENCAR mouse epidermis. Carcinogenesis 22:
1421-7, 2001.
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Tapanadechopone P., Tumova S., Jiang X., Couchman J. R.:
Epidermal transformation leads to increased perlecan synthesis with heparin-binding-growth-factor
affinity. Biochem J 355: 517-27, 2001.
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Weber T. J., Huang Q., Monks T. J., Lau S. S.: Differential
regulation of redox responsive transcription factors by the nephrocarcinogen
2,3,5-tris(glutathion-S-yl)hydroquinone. Chem Res Toxicol 14: 814-21, 2001.
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Yang, H-S., Jansen, A.P., Nair, R., Shibahara, K., Verma,
A.K., Cmarik, J.L. and Colburn, N.H. A novel transformation suppressor,
Pdcd4, inhibits AP-1 transactivation but not NF B or ODC transactivation.
Oncogene 20: 669-676, 2001.
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Young, M.R., Nair, R., Bucheimer, N., Tulsian, P., Hsu, T-C.,
and Colburn, N.H. FRA-1, a pivotal player in the map kinase dependent
activation of AP-1 and neoplastic transformation. MCB, in press.
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Zhang YG, Liu GM, Dong ZG. MSK1 and JNKs mediate phosphorylation
of STAT3 in UVA-irradiated mouse epidermal JB6 cells. J Biol
Chem 276: (45) 42534-42542, 2001.
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Zhong S., Zhang Y., Jansen C., Goto H., Inagaki M., Dong
Z.: MAP Kinases Mediate UVB-induced Phosphorylation of Histone H3 at Serine
28. J Biol Chem 276: 12932-7, 2001.
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