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Hudson, K.

Publications and source records attributed to Hudson, K..

4 recordsLinked to original sources

A first comprehensive analysis of Transcribed Ultra Conserved Regions uncovers important regulatory functions of novel non-coding transcripts in gliomas.

Transcribed Ultra-Conserved Regions (TUCRs) represent a severely understudied class of putative non-coding RNAs (ncRNAs) that are 100% conserved across multiple species. We performed the first-ever analysis of TUCRs in glioblastoma (GBM) and low-grade gliomas (LGG). We leveraged large human datasets to identify the genomic locations, chromatin accessibility, transcription, differential expression, correlation with survival, and predicted functions of all 481 TUCRs, and identified TUCRs that are relevant to glioma biology. Of these, we investigated the expression, function, and mechanism of action of the most highly upregulated intergenic TUCR, uc.110, identifying it as a new tumor enhancer. Uc.110 was highly overexpressed in GBM and LGG, where it promoted malignancy and tumor growth. Uc.110 activated the WNT pathway by upregulating the expression of membrane frizzled-related protein (MFRP), by sponging the tumor suppressor microRNA miR-544. This pioneering study shows important roles for TUCRs in gliomas and provides an extensive database and novel methods for future TUCR research.

cancer biology↗

Genome-wide, Organ-delimited gene regulatory networks (OD-GRNs) provide high accuracy in candidate TF selection across diverse processes.

Construction of organ-specific gene expression datasets that include hundreds to thousands of experiments would greatly aid reconstruction of gene regulatory networks with organ-level spatial resolution. However, creating such datasets is greatly hampered by the requirements of extensive and tedious manual curation. Here we trained a supervised classification model that can accurately classify the organ-of-origin for a plant transcriptome. This K-Nearest Neighbor-based multiclass classifier was used to create organ-specific gene expression datasets for the leaf, root, shoot, flower, seed, seedling, silique, and stem in the model plant Arabidopsis thaliana. In the leaf, root, flower, seed and, a gene regulatory network (GRN) inference approach was used to determine: i. influential transcription factors (TFs) in that organ and, ii. the most influential TFs for specific biological processes in the organ. These genome-wide, organ-delimited GRNs (OD-GRNs), identified de novo many known regulators of organ development and processes operating in those organs. Moreover, many previously unknown TF regulators were highly ranked as potential master regulators of organ development or organ-specific processes. As a proof-of-concept, we focused on experimentally validating the predicted TF regulators of lipid biosynthesis in seeds, with relevance to food and biofuel production. Of the top twenty candidate TFs, eight (e.g., WRI1, LEC1, and FUS3) are known regulators of seed oil content. Importantly, we validated that seven more candidate TFs, whose role was previously unknown in seed lipid biosynthesis, indeed affect this process by genetics and physiological approaches, thus yielding a net accuracy rate of >75% for the de novo TF predictions. The general approach developed here could be extended to any species with sufficiently large gene expression datasets to speed up hypothesis generation and testing for constructing gene regulatory networks at a high spatial resolution. Significance StatementOur study develops a machine-learning framework for building extremely large gene expression datasets for each organ, and to infer organ-delimited gene regulatory networks. We show that this approach is very successful at predicting which transcription factors are going to regulate processes at an organ level. We validated the accuracy of the predictions for transcription factor regulators using the seed lipid synthesis pathway as a case study. We demonstrated a very high success rate for uncovering both known and novel transcription factor regulators for the seed lipid biosynthesis pathway. The approach described in this study is broadly applicable across any organism (plant or animal) that has a large body of public gene expression data.

plant biology↗

Programmed death-ligand 1 expression in human cancer three-dimensional cell culture models

Programmed death-ligand 1 (PD-L1) expression is a survival mechanism employed by tumours to mediate immune evasion and tumour progression. PD-1/PD-L1-targeted therapies have revolutionised the cancer therapy landscape due to their ability to promote durable anti-tumour immune responses in select patients with advanced cancers. However, some patients are unresponsive, hyper-progressive or develop resistance. Better characterisation of the 3D architecture of solid tumours by utilising 3D cell culture could provide an environment that more closely recapitulates in vivo human tumours for investigating tumour-intrinsic PD-L1 signalling and immunotherapy responses. Here we investigated whether PD-L1 expression by human breast, prostate and colorectal cancer cell lines altered in 3D cell culture models compared to their 2D monolayer counterparts. We found that PD-L1 expression changed in 3D-cultured cancer cells when compared to 2D-cultured cells. Additionally, the expression of immunological markers, PD-1, PD-L2, CD44, DR4, DR5, Fas, and HLA-ABC were assessed in 3D cell culture and compared to their expression in 2D. These markers were also altered in 3D compared to 2D-cultured cells, highlighting the importance of utilising 3D models which may better able the investigation of tumour-intrinsic PD-L1 signalling, responses to PD-1/PD-L1-targeted therapy, and combination therapies.

cancer biology↗

A quinolin-8-ol sub-millimolar inhibitor of UGGT, the ER glycoprotein folding quality control checkpoint

The Endoplasmic Reticulum (ER) glycoprotein folding Quality Control (ERQC) machinery aids folding of glycoproteins in the ER. Misfolded glycoprotein recognition and ER-retention is mediated by the ERQC checkpoint enzyme, the 170 kDa UDP-Glucose glycoprotein glucosyltransferase (UGGT). UGGT modulation is a promising strategy for broad-spectrum antivirals, rescue-of-secretion therapy in rare disease caused by responsive mutations in glycoprotein genes, and many cancers, but to date no selective UGGT inhibitors are known. Towards the generation of selective UGGT inhibitors, we determined the crystal structures of the catalytic domain of Chaetomium thermophilum UGGT (CtUGGTGT24), alone and in complex with the inhibitor UDP-2-deoxy-2-fluoro-D-glucose (U2F). Using the CtUGGTGT24 crystals, we carried out a fragment-based lead discovery screen via X-ray crystallography and discovered that the small molecule 5-[(morpholin-4-yl)methyl]quinolin-8-ol (5M-8OH-Q) binds a CtUGGTGT24 WY conserved surface motif that is not present in other GT24 family glycosyltransferases. The 5M-8OH-Q molecule has a 613 {micro}M binding affinity for human UGGT1in vitro as measured by saturation transfer difference NMR spectroscopy. The 5M-8OH-Q molecule inhibits both human UGGT1and UGGT2 activity at concentrations higher than 750 {micro}M in modified HEK293-6E cells. The compound is toxic in cellula and in planta at concentrations higher than 1 mM. A few off-target effects are also observed upon 5M-8OH-Q treatment. Based on an in silico model of the interaction between UGGT and its substrate N -glycan, the 5M-8OH-Q molecule likely works as a competitive inhibitor, binding to the site of recognition of the first GlcNAc residue of the substrate N -glycan. Significance StatementWhen a candidate drug target is the product of a housekeeping gene - i.e. it is important for the normal functioning of the healthy cell - availability of inhibitors for tests and assays is of paramount importance. One such housekeeping protein is UGGT, the enzyme that makes sure that only correctly folded glycoproteins can leave the endoplasmic reticulum for further trafficking through the secretory pathway. UGGT is a potential drug target against viruses, in certain instances of congenital rare disease, and against some cancers, but no UGGT inhibitors are known yet. We discovered and describe here a small molecule that binds human UGGT1 in vitro and inhibits both isoforms of human UGGT in cellula. The compound paves the way to testing of UGGT inhibition as a potential pharmacological strategy in a number of medical contexts.

biochemistry↗