Malignant transformation of simian virus 40-immortalized human milk epithelial cells by chemical carcinogenesis accompanied by loss of heterozygosity on chromosome 1 but not microsatellite instability.

Simian virus 40-immortalized human milk epithelial cells (HuMI) are anchorage dependent and non-tumorigenic but can spontaneously progress to anchorage-independent and tumorigenic cells. To see whether HuMI cells can be transformed into anchorage-independent cells by chemical carcinogens, we treated them with 3-methylcholanthrene (MCA, 10 microg/mL). After 7-8 wk of culture, none of the treated cells grew in soft agar.

Growth inhibition signalled through the interleukin-4/interleukin-13 receptor complex is associated with tyrosine phosphorylation of insulin receptor substrate-1.

Induction of growth inhibition in human colorectal carcinoma cell lines by interleukin (IL)-4 and IL-13 was associated with the neophosphorylation of a 170 kDa cellular protein, identified as insulin receptor substrate-1 (IRS-1) by immunoprecipitation. Tyrosine phosphorylation of IRS-I was also induced by insulin and insulin-like growth factor I. Sublines of colorectal carcinoma cells unresponsive to growth modulation by IL-4, IL-13 or insulin-like growth factor I-induced growth did not phosphorylate IRS-1.

Differential effect of interleukin-4 and transforming growth factor beta 1 on expression of proto-oncogenes and autocrine insulin-like growth factor II in colorectal carcinoma cells.

We have compared the effect of interleukin-4 and transforming growth factor beta 1 on proliferation and gene expression in two colorectal carcinoma cell lines, LS513 and LS1034. Transforming growth factor beta 1 was a potent inhibitor for both cells lines and virtually abolished de novo DNA synthesis. Interleukin-4 inhibited thymidine incorporation up to 60 and 45%, respectively.

Interleukin 4 down-regulates expression of c-kit and autocrine stem cell factor in human colorectal carcinoma cells.

Stem cell factor (SCF) is a cytokine which plays an important role in the development of precursor cells. We have investigated the expression of SCF and its receptor, the c-kit proto-oncogene, in human colorectal carcinoma cell lines. Using reverse transcription-PCR, we confirmed the expression of c-kit in two lines (LS174T and LS1034) and of SCF in 9 of 11 cell lines tested.