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Biology subjects

Wee, K.

Publications and source records attributed to Wee, K..

2 recordsLinked to original sources

Mapping in silico genetic networks of the KMT2D tumour suppressor gene to uncover novel functional associations and cancer cell vulnerabilities

Loss-of-function (LOF) alterations in tumour suppressor genes cannot be directly targeted. Approaches characterising gene function and vulnerabilities conferred by such mutations are required. Here, we computationally map genetic networks of KMT2D, a tumour suppressor gene frequently mutated in several cancer types. Using KMT2D loss-of-function (KMT2DLOF) mutations as a model, we illustrate the utility of in silico genetic networks in uncovering novel functional associations and vulnerabilities in cancer cells with LOF alterations affecting tumour suppressor genes. We revealed genetic interactors with functions in histone modification, metabolism, and immune response, and synthetic lethal (SL) candidates, including some encoding existing therapeutic targets. Analysing patient data from The Cancer Genome Atlas and the Personalized OncoGenomics Project, we showed, for example, elevated immune checkpoint response markers in KMT2DLOF cases, possibly supporting KMT2DLOF as an immune checkpoint inhibitor biomarker. Our study illustrates how tumour suppressor gene LOF alterations can be exploited to reveal potentially targetable cancer cell vulnerabilities.

bioinformatics↗

Snail induces epithelial cell extrusion through transcriptional control of RhoA contractile signalling and cell matrix adhesion

Cell extrusion is a morphogenetic process that is implicated in epithelial homeostasis and highly dependent on the cellular insult and context. Minorities of cells expressing HRasV12 or undergoing apoptosis are typically extruded apically in vertebrate cells. However, basal extrusion (delamination) predominates when mammalian cells express oncogenic KRas and during development in Drosophila. To explore if the morphogenetic transcription factor, Snail, induces extrusion, we inducibly expressed a metabolically stabilized Snail6SA transgene mosaically in confluent MCF-7 monolayers. We found that the morphogenetic impact of Snail6SA was critically influenced by the proportion of cells in which it was expressed. When expressed in small clusters (<3 cells) within confluent monolayers, Snail6SA expression induced apical cell extrusion. In contrast, confluent cultures of Snail6SA expressing cells were retained in the monolayer to eventually undergo basal extrusion (delamination). Transcriptomic profiling revealed that Snail6SA did not substantively alter the balance of epithelial:mesenchymal genes. However, we identified a gene transcriptional network that led to the upregulation of RhoA signalling, actomyosin contractility and reduced basal adhesion in Snail6SA expressing cells. We show that this was necessary to drive both apical extrusion and basal delamination. Thus, contractile upregulation by RhoA along with weakened basal adhesion provides a pathway for Snail to influence epithelial morphogenesis independently of classic Epithelial to Mesenchymal Transition (EMT).

cell biology↗