https://nova.newcastle.edu.au/vital/access/ /manager/Index en-au 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:37515 Wed 23 Aug 2023 09:36:21 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:30575 Wed 20 Mar 2019 12:05:15 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:37757 ARF in human and p19^ARF in mouse) that binds to and inhibits mouse double minute 2 homolog (MDM2) leading to p53 activation, whereas p53 suppresses c-Myc through a combination of mechanisms involving transcriptional inactivation and microRNA-mediated repression. Nonetheless, the regulatory interactions between c-Myc and p53 are not retained by cancer cells as is evident from the often-imbalanced expression of c-Myc over wildtype p53. Although p53 repression in cancer cells is frequently associated with the loss of ARF, we disclose here an alternate mechanism whereby c-Myc inactivates p53 through the actions of the c-Myc-Inducible Long noncoding RNA Inactivating P53 (MILIP). MILIP functions to promote p53 polyubiquitination and turnover by reducing p53 SUMOylation through suppressing tripartite-motif family-like 2 (TRIML2). MILIP upregulation is observed amongst diverse cancer types and is shown to support cell survival, division and tumourigenicity. Thus our results uncover an inhibitory axis targeting p53 through a pan-cancer expressed RNA accomplice that links c-Myc to suppression of p53.]]> Wed 17 Nov 2021 16:28:34 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:32982 Wed 17 Nov 2021 16:28:27 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:31508 Wed 15 Dec 2021 16:08:41 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:19023 V600E or MEK downregulated Noxa, whereas activation of MEK/ERK caused its upregulation. In addition, introduction of BRAF^V600E increased Noxa expression in melanocytes. Upregulation of Noxa was due to a transcriptional increase mediated by cAMP responsive element binding protein, activation of which was also increased by MEK/ERK signaling in melanoma cells. Significantly, Noxa appeared necessary for constitutive activation of autophagy, albeit at low levels, by MEK/ERK in melanoma cells. Furthermore, it was required for autophagy activation that delayed apoptosis in melanoma cells undergoing nutrient deprivation. These results reveal that oncogenic activation of MEK/ERK drives Noxa expression to promote autophagy, and suggest that Noxa has an indirect anti-apoptosis role in melanoma cells under nutrient starvation conditions.]]> Wed 11 Apr 2018 16:41:25 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:28314 Wed 11 Apr 2018 12:40:55 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14353 Wed 11 Apr 2018 11:50:58 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:28216 Wed 11 Apr 2018 09:38:40 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:22865 Wed 11 Apr 2018 09:31:09 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:32985 Wed 10 Nov 2021 15:04:52 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:32181 Wed 09 Mar 2022 15:58:36 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:39074 Wed 04 May 2022 15:24:42 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:28215 Wed 02 Mar 2022 14:25:48 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:35745 chromosome 9 open reading frame 3 gene that was transcriptionally activated by p53. Similarly, the host gene of miRNA-455-3p, collagen alpha-1 (XXVII) chain, was also a p53 transcriptional target. Collectively, our results identify miRNA-27b-3p and miRNA-455-3p as important regulators of cancer cell quiescence in response to p53 and suggest that manipulating miRNA-27b-3p and miRNA-455-3p may constitute novel therapeutic avenues for improving outcomes of cancer treatment. Significance: Two novel p53-responsive microRNAs whose distinct mechanisms of action both stabilize p27 to promote cell quiescence and may serve as therapeutic avenues for improving outcomes of cancer treatment.]]> Thu 28 Oct 2021 12:36:09 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:37758 regenerating islet-derived (REG) gene family are important regulators of many cellular processes. Here we functionally characterise a non-protein coding product of the family, the long noncoding RNA (lncRNA) REG1CP that is transcribed from a DNA fragment at the family locus previously thought to be a pseudogene. REG1CP forms an RNA–DNA triplex with a homopurine stretch at the distal promoter of the REG3A gene, through which the DNA helicase FANCJ is tethered to the core promoter of REG3A where it unwinds double stranded DNA and facilitates a permissive state for glucocorticoid receptor α (GRα)-mediated REG3A transcription. As such, REG1CP promotes cancer cell proliferation and tumorigenicity and its upregulation is associated with poor outcome of patients. REG1CP is also transcriptionally inducible by GRα, indicative of feedforward regulation. These results reveal the function and regulation of REG1CP and suggest that REG1CP may constitute a target for cancer treatment.]]> Thu 27 Jan 2022 15:55:02 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:32504 Thu 14 Apr 2022 10:59:36 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:26954 Sat 24 Mar 2018 07:27:01 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:28221 Fri 16 Oct 2020 16:09:46 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:36768 Fri 03 Jul 2020 14:41:43 AEST ]]>