TGF-β switches from tumor suppressor to prometastatic factor in a model of breast cancer progression
J. Clin. Invest. Binwu Tang, et al. 112:1116 doi:10.1172/JCI18899 [Go to this article.]

Figure 3
Decreased TGF-β responsiveness increases the probability of malignant conversion for the premalignant breast cell line M-II. (a) TGF-β responsiveness of M-II transductants in vitro. The proliferation of M-II transductants in the presence (+) and absence (–) of 2 ng/ml TGF-β1 was determined by incorporation of ³H-thymidine. Results are the mean ± SD of three determinations and are normalized to the no TGF-β control in each case. *P < 0.01. (b) Tumor growth kinetics. Five-week-old female athymic nude mice were inoculated subcutaneously on each hind flank with retrovirally transduced M-II cells (5 × 10⁶ cells/site; ten sites per genotype). (c) Histology of lesions formed by M-II transductants. M-II CON cells formed cystic ductal structures, while MII-DNR formed glandular carcinomas. CON, M-II cells transduced with pLPCX; DNR-pool, pooled M-II cells transduced with pLPC-DNR at levels that fully blocked TGF-β growth-inhibitory responses; DNR-c103, a clone of M-II cells transduced with pLPC-DNR that retained partial TGF-β responsiveness.