ORCID Profile
0000-0003-4592-8358
Current Organisation
University of Adelaide
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Publisher: Hindawi Limited
Date: 2015
DOI: 10.1155/2015/369286
Abstract: The study of immune responses in Drosophila has already yielded significant results with impacts on our understanding of vertebrate immunity, such as the characterization of the Toll receptor. Several recent papers have focused on the humoral response to damage signals rather than pathogens, particularly damage signals from tumour-like tissues generated by loss of cell polarity or chromosomal instability. Both the triggers that generate this sterile inflammation and the systemic and local effects of it are only just beginning to be characterized in Drosophila . Here we review the molecular mechanisms that are known that give rise to the recruitment of Drosophila phagocytes, called hemocytes, as well as the signals, such as TNF α , that stimulated hemocytes emit at sites of perceived damage. The signalling consequences of inflammation, such as the activation of JNK, and the potential for modifying this response are also discussed.
Publisher: Springer New York
Date: 2018
DOI: 10.1007/978-1-4939-7562-4_8
Abstract: Circular RNAs (circRNAs) constitute an emerging class of widespread, abundant, and evolutionarily conserved noncoding RNA. They play important and erse roles in cell development, growth, and tumorigenesis, but functions of the majority of circRNAs remain enigmatic. In order to investigate circRNA function it is necessary to manipulate its expression. While various standard approaches exist for circRNA knockdown, here we present cloning vectors for simplifying the laborious process of cloning circRNAs to achieve high-efficiency overexpression in mammalian cell lines.
Publisher: Impact Journals, LLC
Date: 31-08-2016
Publisher: EMBO
Date: 06-06-2018
Publisher: Georg Thieme Verlag KG
Date: 05-2015
Abstract: Chromosomal instability (CIN) is a common feature of tumours that leads to increased genetic ersity in the tumour and poor clinical outcomes. There is considerable interest in understanding how CIN comes about and how its contribution to drug resistance and metastasis might be counteracted. In the last decade a number of CIN model systems have been developed in Drosophila that offer unique benefits both in understanding the development of CIN in a live animal as well as giving the potential to do genome wide screens for therapeutic candidate genes. This review outlines the mechanisms used in several Drosophila CIN model systems and summarizes some significant outcomes and opportunities that they have produced.
Publisher: Elsevier BV
Date: 07-2023
Publisher: MDPI AG
Date: 23-10-2021
Abstract: Circular RNAs are regulatory molecules involved in numerous cellular processes and may be involved in tumour growth and diffusion. Here, we define the expression of 15 selected circular RNAs, which may control the process of epithelial-to-mesenchymal transition, using a panel of 18 breast cancer cell lines recapitulating the heterogeneity of these tumours and consisting of three groups according to the mesenchymal/epithelial phenotype. A circular RNA from the DOCK1 gene (hsa_circ_0020397) shows low/undetectable levels in triple-negative mesenchymal cell lines, while its content is high in epithelial cell lines, independent of estrogen receptor or HER2 positivity. RNA-sequencing experiments performed on the triple-negative/mesenchymal MDA-MB-231 and MDA-MB-157 cell lines engineered to overexpress hsa_circ_0020397 demonstrate that the circRNA influences the expression of 110 common genes. Pathway analysis of these genes indicates that overexpression of the circular RNA differentiates the two mesenchymal cell lines along the epithelial pathway and increases cell-to-cell adhesion. This is accompanied by growth inhibition and a reduction in the random/directional motility of the cell lines. The upregulated AGR2, ENPP1, and PPP1R9A genes as well as the downregulated APOE, AQP3, CD99L2, and IGFBP4 genes show an opposite regulation by hsa_circ_0020397 silencing in luminal CAMA1 cells. The results provide novel insights into the role played by specific circular RNAs in the generation rogression of breast cancer.
Publisher: Bentham Science Publishers Ltd.
Date: 05-01-2016
DOI: 10.2174/1389450116666150126111055
Abstract: The production of reactive oxygen species is a normal part of cell physiology, but many internal and external stimuli are able to trigger the production of excess levels of oxidants that are potentially damaging. The threat of oxidative damage is particularly significant to DNA, as damaged bases can interfere with replication to generate lasting mutations. Signalling through the JNK pathway is a key cellular response to oxidative damage. Depending on the intensity and duration of the damage signal, JNK signalling can lead to distinct alternative responses including DNA repair, anti-oxidant production or cell death. These responses are highly relevant to cancer therapy, as tumours are often under oxidative stress that produces elevated JNK levels and therapy often involves inducing DNA damage with the intention of driving cell death. In this review we examine the causes and consequences of JNK activation that relate to oxidative DNA damage, with a focus on the potential therapeutic implications.
Publisher: Impact Journals, LLC
Date: 10-10-2015
Publisher: Springer Science and Business Media LLC
Date: 27-10-2015
DOI: 10.1038/ONC.2014.344
Abstract: Chromosomal INstability (CIN), a hallmark of cancer, refers to cells with an increased rate of gain or loss of whole chromosomes or chromosome parts. CIN is linked to the progression of tumors with poor clinical outcomes such as drug resistance. CIN can give tumors the ersity to resist therapy, but it comes at the cost of significant stress to tumor cells. To tolerate this, cancer cells must modify their energy use to provide adaptation against genetic changes as well as to promote their survival and growth. In this study, we have demonstrated that CIN induction causes sensitivity to metabolic stress. We show that mild metabolic disruption that does not affect normal cells, can lead to high levels of oxidative stress and subsequent cell death in CIN cells because they are already managing elevated stress levels. Altered metabolism is a differential characteristic of cancer cells, so our identification of key regulators that can exploit these changes to cause cell death may provide cancer-specific potential drug targets, especially for advanced cancers that exhibit CIN.
Publisher: Oxford University Press (OUP)
Date: 31-07-2023
DOI: 10.1093/NAR/GKAD645
Abstract: MiRNAs post-transcriptionally repress gene expression by binding to mRNA 3′UTRs, but the extent to which they act through protein coding regions (CDS regions) is less well established. MiRNA interaction studies show a substantial proportion of binding occurs in CDS regions, however sequencing studies show much weaker effects on mRNA levels than from 3′UTR interactions, presumably due to competition from the translating ribosome. Consequently, most target prediction algorithms consider only 3′UTR interactions. However, the consequences of CDS interactions may have been underestimated, with the reporting of a novel mode of miRNA-CDS interaction requiring base pairing of the miRNA 3′ end, but not the canonical seed site, leading to repression of translation with little effect on mRNA turnover. Using extensive reporter, western blotting and bioinformatic analyses, we confirm that miRNAs can indeed suppress genes through CDS-interaction in special circumstances. However, in contrast to that previously reported, we find repression requires extensive base-pairing, including of the canonical seed, but does not strictly require base pairing of the 3′ miRNA terminus and is mediated through reducing mRNA levels. We conclude that suppression of endogenous genes can occur through miRNAs binding to CDS, but the requirement for extensive base-pairing likely limits the regulatory impacts to modest effects on a small subset of targets.
No related grants have been discovered for Dawei Liu.