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Articles

The anion channel GPR89 is a tumor-specific dependency in breast cancer

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By Riccardo Ferro, Alexandra Nicewicz Carroll, Virinder Reen, George Vlachogiannis, Rebeca Uceda-Castro, Dragomir B. Krastev, Valeria Amodeo, Stephen Pettitt, Nadja D’Uonno, Ioanna Mavrommati, Blanca Navarro, Luke Hitchen, Jennifer Trendell, Ana Stojiljkovic, Cynthia Prince, Ioannis Roxanis, Patrycja Gazinska, Daniel Larcombe-Young, Rebecca Marlow, Stefano Annunziato, Jos Jonkers, Nalan Liv, John Alexander, Jelmar S. Quist, Mercedes Pardo, Theodoros I. Roumeliotis, Jyoti Choudhary, Daniel Weekes, Joanna I Loizou, Rachael Natrajan, Anita Grigoriadis, Syed Imran Haider, Christopher Lord Verified, Andrew Tutt, Ana M. Mendes-Pereira, Narinder Janghra, Tejashree Rajaram Kanitkar, Amadeus Xu, Nirmesh Patel, Pierfrancesco Marra, Mallur Srivatsan Madhusudhan
| Nature Verified
Abstract How cancers regulate endoplasmic reticulum (ER) pH and minimize ER stress remains unclear. Here we show that in breast cancer, these processes are governed by the anion channel GPR89. While normally localized to the Golgi, we find GPR89 is also present in the ER of tumor cells, where it collaborates with vacuolar H⁺ ATPase to regulate pH, and reduces ER stress via IRE1α-HSP47-XBP1s, ATF6 and ATP2A2 pathways.
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Tumour specific HORMAD1 expression perturbs mitotic arrest and drives sensitivity to mitotic kinase inhibitors

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By Callum Walker, Jennifer Trendell, Ricarda Hoffmann, Alexia Martin, Blanca Navarro-Llinas, Mercedes Calvo, Nicolae Balan, Harriet I. Kemp, Alexandra Nicewicz Carroll, Kathryn Davidson, Ruifang Lu, Chris Starling, Nino Iakobachvili, Jelmar S. Quist, Lu Yu, Dragomir B. Krastev, Valeria Amodeo, Ioannis Roxanis, Anita Grigoriadis, Richard Bayliss, Jyoti Choudhary, Syed Imran Haider, Jonathon Pines, Stephen Pettitt, Christopher Lord Verified, Andrew Tutt, Gabriel Kollarovic, Daniel Weekes, Riccardo Ferro, Luke Hitchen, Sarmi Nath, Nadja D’Uonno, Marieke Otten, Chiara Marcozzi, Ilhan Rahman
| Nature Verified
Abstract HORMAD1 expression is usually restricted to germ-line cells but is also aberrantly expressed in 60% of triple-negative breast cancers (TNBCs), where it is bi-modally expressed and associated with genomic instability. Here, we show that out-of-context HORMAD1 expression in mitotic cells perturbs mitotic arrest and generates aneuploidy.
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The transcriptomic architecture of common cancers reflects synthetic lethal interactions - Nature Genetics

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By Syed Imran Haider, Santiago Madera, Andrew J. Wicks, Stephen Pettitt
| Nature Verified
Abstract To maintain cell fitness, deleterious genetic alterations are buffered by compensatory changes in additional genes. In cancer, buffering processes could be targeted by synthetic lethality. However, despite the large-scale identification of synthetic lethal effects in preclinical models, evidence that these operate clinically is limited. This impedes the application of synthetic lethal approaches.
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