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TGF-beta 1 is an autocrine-negative growth regulator of human colon carcinoma FET cells in vivo as revealed by transfection of an antisense expression vector.
Open accessAbstract
Transforming growth factor-beta 1 (TGF-beta 1) has previously been implicated as a potential negative autocrine or paracrine growth regulator of certain cell types (Arteaga, C. L., R. J. Coffey, Jr., T. C. Dugger, C. M. McCutchen, H. L. Moses, and R. M. Lyons. 1990. Cell Growth & Differ. 1:367-374; Hafez, M. M., D. Infante, S. Winawer, and E. Friedman. 1990. Cell Growth & Differ. 1:617-626; Glick, A. B., K. C. Flanders, D. Danielpour, S. H. Yuspa, and M. B. Sporn. 1989. Cell Regulation. 1:87-97). This is based mainly on experiments assessing the effects of exogenous TGF-beta 1 or neutralizing antibodies to TGF-beta 1 on normal or tumor cell proliferation in vitro. However, direct evidence demonstrating such a negative regulation of tumor cell growth in vivo is still lacking. To overcome this problem we have constructed and used an antisense expression vector for TGF-beta 1 as a means of regulating endogenous TGF-beta 1 expression in tumor cells. Antisense-transfected FET human colon carcinoma cells showed a fivefold reduction in TGF-beta 1 mRNA and 15-fold reduction in TGF-beta 1 secretion. Antisense mRNA was detected in transfected cells by an RNase protection assay. Compared to control cells, cultured antisense-transfected cells showed a reduction in lag phase time rather than a change in doubling time. Cloning efficiencies of transfected cells were four times greater than control cells in anchorage-independent assays. Control cells did not form tumors at 5 x 10(5) in athymic nude mice. Antisense-transfected cells formed tumors in 40% of animals injected. At higher inocula (1 x 10(6) cells) antisense-transfected cells formed tumors in 100% of animals injected, but control cells still failed to form tumors. These results show that TGF-beta 1 acts as a negative growth regulator of human colon carcinoma cells in vivo as well as in vitro. Acquisition of partial or full resistance to such inhibitory effects may therefore contribute to tumor development and progression.
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Citations
Cited by
TGF-β and the TGF-β family: context-dependent roles in cell and tissue physiology
Morikawa, M., Derynck, R., & Miyazono, K. (2016) · Cold Spring Harbor Perspectives in Biology · doi:10.1101/cshperspect.a021873 · Cited by 1,321
Transforming growth factor-beta: recent progress and new challenges.
Sporn, M. B., & Roberts, A. B. (1992) · The Journal of cell biology · doi:10.1083/jcb.119.5.1017 · Cited by 769
Cui, W., Fowlis, D. J., Bryson, S., Duffie, E., Ireland, H., Balmain, A., & Akhurst, R. J. (1996) · Cell · doi:10.1016/s0092-8674(00)80127-0 · Cited by 628
Tumor suppressor activity of the TGF-β pathway in human cancers
Markowitz, S. (1996) · Cytokine & Growth Factor Reviews · doi:10.1016/1359-6101(96)00001-9 · Cited by 416
Arteaga, C. L., Hurd, S. D., Winnier, A. R., Johnson, M. D., Fendly, B. M., & Forbes, J. T. (1993) · Journal of Clinical Investigation · doi:10.1172/jci116871 · Cited by 359
Metadata
- Authors
- Wu, S. P., Theodorescu, D., Kerbel, R. S., Willson, J. K., Mulder, K. M., Humphrey, L. E., & Brattain, M. G.
- Venue
- The Journal of cell biology
- Publisher
- Rockefeller University Press
- Published
- 1992-01-01
- Volume
- 116
- Issue
- 1
- Pages
- 187-196
- ISSN
- 0021-9525 (ISSN-L)
- 1540-8140
- OpenAlex
- W2025806580
- Cited by
- 180
- References
- 0
- FWCI
- 6.87
- Type
- journal article
- Language
- en
- Open access
- green
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- CoChat. (2026). Citation check: TGF-beta 1 is an autocrine-negative growth regulator of human colon carcinoma FET cells in vivo as revealed by transfection of an antisense expression vector. https://app.cochat.ai/papers/10.1083/jcb.116.1.187
- The paper
- Wu, S. P., Theodorescu, D., Kerbel, R. S., Willson, J. K., Mulder, K. M., Humphrey, L. E., & Brattain, M. G. (1992). TGF-beta 1 is an autocrine-negative growth regulator of human colon carcinoma FET cells in vivo as revealed by transfection of an antisense expression vector. The Journal of cell biology. https://doi.org/10.1083/jcb.116.1.187
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