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Following Epo stimulation, we investigated EpoR's ability to promote tumor formation and invasiveness. Comparing parental Rama 37 cells, which contain few or no endogenous EpoRs, and a human EpoR-stably transfected with a modified cell line stably transfected with human EpoR, showed cell signaling and malignant cell behavior. Incubation of Rama 37-28 cells with Epo pharmacologic levels resulted in the rapid and sustained rises in phosphorylation of signal transducers and activators of transcription 5, Akt, and extracellular signal-regulated kinase. Epo causes phenotypic changes in breast cancer cell lines' behavior and establishes links between individual cell signaling pathways and tumor spread, according to these results.
Source link: https://doi.org/10.1158/1541-7786.mcr-09-0264
In vitro and in vivo, we investigated the effects of JMR-132, the GHRH antagonist, on PC-3 human androgen-independent prostate cancer cells. JMR-132 stopped PC-3 cell proliferation in vitro in a dose-dependent manner and dramatically reduced PC-3 tumor formation by 61%. By RT-PCR and Western blot, the expression of GHRH, and their main splice variant, SV1, was demonstrated in PC-3 cells and tumor xenografts. After starting JMR-132 treatment, the GHRH protein content in PC-3 xenografts was reduced sharply by 66. 3 percent. In part, the inhibitory effect produced by GHRH antagonist may have arisen in part due to the activation of the PI3K/Akt/Mammalian target of rapamycin and Raf/ERK pathways and the reduction of GHRH produced by cancer cells. Our results support the role of GHRH as an autocrine growth factor in prostate cancer, and we recommend that antagonists of GHRH be considered further as a treatment for CRPC.
Source link: https://doi.org/10.1073/pnas.1120588109
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