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Tumour necrosis factor alpha (cachectin) mimics some of the effects of tumour growth on the disposal of a [14C]lipid load in virgin, lactating and litter-removed rats.

ABSTRACT: Tumour necrosis factor alpha (cachectin) was administered to virgin, lactating and litter-removed rats, and subsequent disposal of an oral [1-14C]triolein (glycerol tri[1-14C]oleate) load examined. Absorption of the lipid and 14CO2 production were significantly depressed in all three groups. [14C]Lipid accumulation was decreased in carcass, liver and adipose tissue (brown and white) of virgin and litter-removed rats and the mammary gland of lactating rats. The plasma triacylglycerol concentration was increased in all three groups, and lipoprotein lipase activity was decreased in the white adipose tissue of virgin and litter-removed animals and in the mammary gland of lactating animals. Some, but not all, of these effects mimic tumour burden in the same physiological states [Evans & Williamson (1988) Biochem. J. 252, 65-72].

SUBMITTER: Evans RD

PROVIDER: S-EPMC1135525 | biostudies-other | 1988 Dec

REPOSITORIES: biostudies-other

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Project description:BackgroundData from in vivo and in vitro studies suggest that activation of Akt regulates cell survival signaling and plays a key role in tumorigenesis. Hence, transgenic mice were created to explore the oncogenic role of Akt1 in the development of mammary tumors.MethodsThe transgenic mice were generated by expressing myristoylated-Akt1 (myr-Akt1) under the control of the MMTV-LTR promoter. The carcinogen 7, 12 dimethyl-1,2-benzanthracene (DMBA) was used to induce tumor formation.ResultsThe MMTV driven myr-Akt1 transgene expression was detected primarily in the mammary glands, uterus, and ovaries. The expression level increased significantly in lactating mice, suggesting that the response was hormone dependent. The total Akt expression level in the mammary gland was also higher in the lactating mice. Interestingly, the expression of MMTVmyr-Akt1 in the ovaries of the transgenic mice caused significant increase in circulating estrogen levels, even at the post-lactation stage. Expression of myr-Akt1 in mammary glands alone did not increase the frequency of tumor formation. However, there was an increased susceptibility of forming mammary tumors induced by DMBA in the transgenic mice, especially in mice post-lactation. Within 34 weeks, DMBA induced mammary tumors in 42.9% of transgenic mice post-lactation, but not in wild-type mice post-lactation. The myr-Akt1 mammary tumors induced by DMBA had increased phosphorylated-Akt1 and showed strong expression of estrogen receptor (ER?) and epidermal growth factor receptor (EGFR). In addition, Cyclin D1 was more frequently up-regulated in mammary tumors from transgenic mice compared to tumors from wild-type mice. Overexpression of Cyclin D1, however, was not completely dependent on activated Akt1. Interestingly, mammary tumors that had metastasized to secondary sites had increased expression of Twist and Slug, but low expression of Cyclin D1.ConclusionsIn summary, the MMTVmyr-Akt1 transgenic mouse model could be useful to study mechanisms of ER-positive breast tumor development.

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Tumour necrosis factor alpha (cachectin) mimics some of the effects of tumour growth on the disposal of a [14C]lipid load in virgin, lactating and litter-removed rats.

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