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2. Author Correction: Cytoskeleton remodeling induced by SMYD2 methyltransferase drives breast cancer metastasis

Author

Casanova, Alexandre G., Roth, Gael S., Hausmann, Simone, Lu, Xiaoyin, Bischoff, Ludivine J. M., Froeliger, Emilie M., Belmudes, Lucid, Bourova-Flin, Ekaterina, Flores, Natasha M., Benitez, Ana Morales, Chasan, Tourkian, Caporicci, Marcello, Vayr, Jessica, Blanchet, Sandrine, Ielasi, Francesco, Rousseaux, Sophie, Hainaut, Pierre, Gozani, Or, Le Romancer, Muriel, Couté, Yohann, Palencia, Andres, Mazur, Pawel K., and Reynoird, Nicolas

Published
2024
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3. Cytoskeleton remodeling induced by SMYD2 methyltransferase drives breast cancer metastasis

Author

Casanova, Alexandre G., Roth, Gael S., Hausmann, Simone, Lu, Xiaoyin, Bischoff, Ludivine J. M., Froeliger, Emilie M., Belmudes, Lucid, Bourova-Flin, Ekaterina, Flores, Natasha M., Benitez, Ana Morales, Chasan, Tourkian, Caporicci, Marcello, Vayr, Jessica, Blanchet, Sandrine, Ielasi, Francesco, Rousseaux, Sophie, Hainaut, Pierre, Gozani, Or, Le Romancer, Muriel, Couté, Yohann, Palencia, Andres, Mazur, Pawel K., and Reynoird, Nicolas

Published
2024
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6. Elevated NSD3 histone methylation activity drives squamous cell lung cancer

Author

Yuan, Gang, Flores, Natasha M., Hausmann, Simone, Lofgren, Shane M., Kharchenko, Vladlena, Angulo-Ibanez, Maria, Sengupta, Deepanwita, Lu, Xiaoyin, Czaban, Iwona, Azhibek, Dulat, Vicent, Silvestre, Fischle, Wolfgang, Jaremko, Mariusz, Fang, Bingliang, Wistuba, Ignacio I., Chua, Katrin F., Roth, Jack A., Minna, John D., Shao, Ning-Yi, Jaremko, Łukasz, Mazur, Pawel K., and Gozani, Or

Published
2021
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7. Cytoskeleton remodeling induced by SMYD2 methyltransferase drives breast cancer metastasis

Author

Casanova, Alexandre G, primary, Roth, Gael S, additional, Hausmann, Simone, additional, Lu, Xiaoyin, additional, Belmudes, Lucid, additional, Bourova-Flin, Ekaterina, additional, Flores, Natasha M, additional, Benitez, Ana Morales, additional, Caporicci, Marcello, additional, Vayr, Jessica, additional, Blanchet, Sandrine, additional, Ielasi, Francesco, additional, Rousseaux, Sophie, additional, Hainaut, Pierre, additional, Gozani, Or, additional, Coute, Yohann, additional, Palencia, Andres, additional, Mazur, Pawel K, additional, and Reynoird, Nicolas, additional

Published
2023
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9. Comprehensive molecular phenotyping ofARID1A-deficient gastric cancer reveals pervasive epigenomic reprogramming and therapeutic opportunities

Author

Xu, Chang, primary, Huang, Kie Kyon, additional, Law, Jia Hao, additional, Chua, Joy Shijia, additional, Sheng, Taotao, additional, Flores, Natasha M, additional, Pizzi, Melissa Pool, additional, Okabe, Atsushi, additional, Tan, Angie Lay Keng, additional, Zhu, Feng, additional, Kumar, Vikrant, additional, Lu, Xiaoyin, additional, Benitez, Ana Morales, additional, Lian, Benedict Shi Xiang, additional, Ma, Haoran, additional, Ho, Shamaine Wei Ting, additional, Ramnarayanan, Kalpana, additional, Anene-Nzelu, Chukwuemeka George, additional, Razavi-Mohseni, Milad, additional, Abdul Ghani, Siti Aishah Binte, additional, Tay, Su Ting, additional, Ong, Xuewen, additional, Lee, Ming Hui, additional, Guo, Yu Amanda, additional, Ashktorab, Hassan, additional, Smoot, Duane, additional, Li, Shang, additional, Skanderup, Anders Jacobsen, additional, Beer, Michael A, additional, Foo, Roger Sik Yin, additional, Wong, Joel Shi Hao, additional, Sanghvi, Kaushal, additional, Yong, Wei Peng, additional, Sundar, Raghav, additional, Kaneda, Atsushi, additional, Prabhakar, Shyam, additional, Mazur, Pawel Karol, additional, Ajani, Jaffer A, additional, Yeoh, Khay Guan, additional, So, Jimmy Bok-Yan, additional, and Tan, Patrick, additional

Published
2023
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12. Comprehensive molecular phenotyping of ARID1A-deficient gastric cancer reveals pervasive epigenomic reprogramming and therapeutic opportunities

Author

Xu, Chang, Huang, Kie Kyon, Law, Jia Hao, Chua, Joy Shijia, Sheng, Taotao, Flores, Natasha M, Pizzi, Melissa Pool, Okabe, Atsushi, Tan, Angie Lay Keng, Zhu, Feng, Kumar, Vikrant, Lu, Xiaoyin, Benitez, Ana Morales, Lian, Benedict Shi Xiang, Ma, Haoran, Ho, Shamaine Wei Ting, Ramnarayanan, Kalpana, Anene-Nzelu, Chukwuemeka George, Razavi-Mohseni, Milad, Abdul Ghani, Siti Aishah Binte, Tay, Su Ting, Ong, Xuewen, Lee, Ming Hui, Guo, Yu Amanda, Ashktorab, Hassan, Smoot, Duane, Li, Shang, Skanderup, Anders Jacobsen, Beer, Michael A, Foo, Roger Sik Yin, Wong, Joel Shi Hao, Sanghvi, Kaushal, Yong, Wei Peng, Sundar, Raghav, Kaneda, Atsushi, Prabhakar, Shyam, Mazur, Pawel Karol, Ajani, Jaffer A, Yeoh, Khay Guan, So, Jimmy Bok-Yan, and Tan, Patrick

Abstract

ObjectiveGastric cancer (GC) is a leading cause of cancer mortality, with ARID1Abeing the second most frequently mutated driver gene in GC. We sought to decipher ARID1A-specific GC regulatory networks and examine therapeutic vulnerabilities arising from ARID1Aloss.DesignGenomic profiling of GC patients including a Singapore cohort (>200 patients) was performed to derive mutational signatures of ARID1Ainactivation across molecular subtypes. Single-cell transcriptomic profiles of ARID1A-mutated GCs were analysed to examine tumour microenvironmental changes arising from ARID1Aloss. Genome-wide ARID1A binding and chromatin profiles (H3K27ac, H3K4me3, H3K4me1, ATAC-seq) were generated to identify gastric-specific epigenetic landscapes regulated by ARID1A. Distinct cancer hallmarks of ARID1A-mutated GCs were converged at the genomic, single-cell and epigenomic level, and targeted by pharmacological inhibition.ResultsWe observed prevalent ARID1Ainactivation across GC molecular subtypes, with distinct mutational signatures and linked to a NFKB-driven proinflammatory tumour microenvironment. ARID1A-depletion caused loss of H3K27ac activation signals at ARID1A-occupied distal enhancers, but unexpectedly gain of H3K27ac at ARID1A-occupied promoters in genes such as NFKB1and NFKB2. Promoter activation in ARID1A-mutated GCs was associated with enhanced gene expression, increased BRD4 binding, and reduced HDAC1 and CTCF occupancy. Combined targeting of promoter activation and tumour inflammation via bromodomain and NFKB inhibitors confirmed therapeutic synergy specific to ARID1A-genomic status.ConclusionOur results suggest a therapeutic strategy for ARID1A-mutated GCs targeting both tumour-intrinsic (BRD4-assocatiated promoter activation) and extrinsic (NFKB immunomodulation) cancer phenotypes.

Published
2023
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23. Effects of individually silenced N-glycosylation sites and non-synonymous single-nucleotide polymorphisms on the fusogenic function of human syncytin-2

Author

Cui, Lina, primary, Wang, Huiying, additional, Lu, Xiaoyin, additional, Wang, Rui, additional, Zheng, Ru, additional, Li, Yue, additional, Yang, Xiaokui, additional, Jia, Wen-Tong, additional, Zhao, Yangyu, additional, Wang, Yongqing, additional, Wang, Haibin, additional, Wang, Yan-Ling, additional, Zhu, Cheng, additional, Lin, Hai-Yan, additional, and Wang, Hongmei, additional

Published
2016
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29. Atlas of Metastatic Gastric Cancer Links Ferroptosis to Disease Progression and Immunotherapy Response.

Author

Cheng X, Dai E, Wu J, Flores NM, Chu Y, Wang R, Dang M, Xu Z, Han G, Liu Y, Chatterjee D, Hu C, Ying J, Du Y, Yang L, Guan X, Mo S, Cao X, Pei G, Jiang J, Lu X, Benitez AM, Waters RE, Pizzi MP, Shanbhag N, Fan Y, Peng F, Hanash SM, Calin G, Futreal A, Song S, Yee C, Mazur PK, Qin JJ, Ajani JA, and Wang L

Abstract

Background & Aims: Metastases from gastric adenocarcinoma (GAC) lead to high morbidity and mortality. Developing innovative and effective therapies requires a comprehensive understanding of the tumor and immune biology of advanced GAC. Yet, collecting matched specimens from advanced, treatment-naïve patients with GAC poses a significant challenge, limiting the scope of current research, which has focused predominantly on localized tumors. This gap hinders deeper insight into the metastatic dynamics of GAC., Methods: We performed in-depth single-cell transcriptome and immune profiling on 68 paired, treatment-naïve, primary metastatic tumors to delineate alterations in cancer cells and their tumor microenvironment during metastatic progression. To validate our observations, we conducted comprehensive functional studies both in vitro and in vivo, using cell lines and multiple patient-derived xenograft and novel mouse models of GAC., Results: Liver and peritoneal metastases exhibited distinct properties in cancer cells and dynamics of tumor microenvironment phenotypes, supporting the notion that cancer cells and their local tumor microenvironments co-evolve at metastatic sites. Our study also revealed differential activation of cancer meta-programs across metastases. We observed evasion of cancer cell ferroptosis via GPX4 up-regulation during GAC progression. Conditional depletion of Gpx4 or pharmacologic inhibition of ferroptosis resistance significantly attenuated tumor growth and metastatic progression. In addition, ferroptosis-resensitizing treatments augmented the efficacy of chimeric antigen receptor T-cell therapy., Conclusions: This study represents the largest single-cell dataset of metastatic GACs to date. High-resolution mapping of the molecular and cellular dynamics of GAC metastasis has revealed a rationale for targeting ferroptosis defense in combination with chimeric antigen receptor T-cell therapy as a novel therapeutic strategy with potential immense clinical implications., (Copyright © 2024 AGA Institute. Published by Elsevier Inc. All rights reserved.)

Published
2024
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30. Cytoskeleton remodeling induced by SMYD2 methyltransferase drives breast cancer metastasis.

Author

Casanova AG, Roth GS, Hausmann S, Lu X, Belmudes L, Bourova-Flin E, Flores NM, Benitez AM, Caporicci M, Vayr J, Blanchet S, Ielasi F, Rousseaux S, Hainaut P, Gozani O, Couté Y, Palencia A, Mazur PK, and Reynoird N

Abstract

Malignant forms of breast cancer refractory to existing therapies remain a major unmet health issue, primarily due to metastatic spread. A better understanding of the mechanisms at play will provide better insights for alternative treatments to prevent breast cancer cells dispersion. Here, we identify the lysine methyltransferase SMYD2 as a clinically actionable master regulator of breast cancer metastasis. While SMYD2 is overexpressed in aggressive breast cancers, we notice that it is not required for primary tumor growth. However, mammary-epithelium specific SMYD2 ablation increases mouse overall survival by blocking the primary tumor cells ability to metastasize. Mechanistically, we identify BCAR3 as a genuine physiological substrate of SMYD2 in breast cancer cells. BCAR3 monomethylated at lysine K334 (K334me1) is recognized by a novel methyl-binding domain present in FMNLs proteins. These actin cytoskeleton regulators are recruited at the cell edges by the SMYD2 methylation signaling and modulates lamellipodia properties. Breast cancer cells with impaired BCAR3 methylation loose migration and invasiveness capacity in vitro and are ineffective in promoting metastases in vivo . Remarkably, SMYD2 pharmacologic inhibition efficiently impairs the metastatic spread of breast cancer cells, PDX and aggressive mammary tumors from genetically engineered mice. This study provides a rationale for innovative therapeutic prevention of malignant breast cancer metastatic progression by targeting the SMYD2-BCAR3-FMNL axis.

Published
2023
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31. Deep RNA sequencing analysis of syncytialization-related genes during BeWo cell fusion.

Author

Zheng R, Li Y, Sun H, Lu X, Sun BF, Wang R, Cui L, Zhu C, Lin HY, and Wang H

Abstract

The syncytiotrophoblast (STB) plays a key role in maintaining the function of the placenta during human pregnancy. However, the molecular network that orchestrates STB development remains elusive. The aim of this study was to obtain broad and deep insight into human STB formation via transcriptomics. We adopted RNA sequencing (RNA-Seq) to investigate genes and isoforms involved in forskolin (FSK)-induced fusion of BeWo cells. BeWo cells were treated with 50 μM FSK or dimethylsulfoxide (DMSO) as a vehicle control for 24 and 48 h, and the mRNAs at 0, 24 and 48 h was sequenced. We detected 28,633 expressed genes and identified 1,902 differentially expressed genes (DEGs) after FSK treatment for 24 and 48 h. Among the 1,902 DEGs, 461 were increased and 395 were decreased at 24 h, while 879 were up-regulated and 763 were down-regulated at 48 h. When the 856 DEGs identified at 24 h were traced individually at 48 h, they separated into 6 dynamic patterns via a K-means algorithm, and most were enriched in down-even and up-even patterns. Moreover, the Gene Ontology (GO) terms syncytium formation, cell junction assembly, cell fate commitment, calcium ion transport, regulation of epithelial cell differentiation and cell morphogenesis involved in differentiation were clustered, and the MAPK pathway was most significantly regulated. Analyses of alternative splicing isoforms detected 123,200 isoforms, of which 1,376 were differentially expressed. The present deep analysis of the RNA-Seq data of BeWo cell fusion provides important clues for understanding the mechanisms underlying human STB formation.

Published
2016
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