https://ogma.newcastle.edu.au/vital/access/ /manager/Index en-au 5 ACTN4 regulates the stability of RIPK1 in melanoma https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:37515 Wed 23 Aug 2023 09:36:21 AEST ]]> c-Myc inactivation of p53 through the pan-cancer lncRNA MILIP drives cancer pathogenesis https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:37757 ARF in human and p19ARF 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 ]]> Noxa upregulation by oncogenic activation of MEK/ERK through CREB promotes autophagy in human melanoma cells https://ogma.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 BRAFV600E 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 ]]> RIPK1 regulates survival of human melanoma cells upon endoplasmic reticulum stress through autophagy https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:28314 Wed 11 Apr 2018 12:40:55 AEST ]]> INPP4B is upregulated and functions as an oncogenic driver through SGK3 in a subset of melanomas https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:22865 Wed 11 Apr 2018 09:31:09 AEST ]]> Cylindromatosis is required for survival of a subset of melanoma cells https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:39074 Wed 04 May 2022 15:24:42 AEST ]]> The pan-cancer lncRNA PLANE regulates an alternative splicing program to promote cancer pathogenesis https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:45314 Thu 27 Oct 2022 13:56:29 AEDT ]]> The double life of RIPK1 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:50344 Thu 20 Jul 2023 14:26:55 AEST ]]> RIP1 kinase is an oncogenic driver in melanoma https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:26954 Sat 24 Mar 2018 07:27:01 AEDT ]]> RIP1 protects melanoma cells from apoptosis induced by BRAF/MEK inhibitors https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:36768 Fri 03 Jul 2020 14:41:43 AEST ]]>