ArticleBMC cancer2014
Activation of Akt1 accelerates carcinogen-induced tumorigenesis in mammary gland of virgin and post-lactating transgenic mice.
Article in BMC cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- AKT kinases as therapeutic targets.Journal of experimental & clinical cancer research : CR · 2024Review
- Unraveling molecular characteristics and tumor microenvironment dynamics of neuroendocrine prostate cancer.Journal of cancer research and clinical oncology · 2024Review
- Effect of AKT silence on malignant biological behavior of renal cell carcinoma cells.BMC urology · 2022Article
- The AKT1E17K Allele Promotes Breast Cancer in Mice.Cancers · 2022Article
- Emerging Roles for AKT Isoform Preference in Cancer Progression Pathways.Molecular cancer research : MCR · 2021Review
- Expression of MALAT1 Promotes Trastuzumab Resistance in HER2 Overexpressing Breast Cancers.Cancers · 2020Article
- The unconventional role of Akt1 in the advanced cancers and in diabetes-promoted carcinogenesis.Pharmacological research · 2019Review
- Phosphorylated Akt1 expression is associated with poor prognosis in cutaneous, oral and sinonasal melanomas.Oncotarget · 2018Article
- A83-01 inhibits TGF-β-induced upregulation of Wnt3 and epithelial to mesenchymal transition in HER2-overexpressing breast cancer cells.Breast cancer research and treatment · 2017Article
Corrections and comments
- Retracted
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
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 (ERα) 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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