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Ömer An

National University Cancer Institute, Singapore

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Henry Yang

National University of Singapore

Leilei Chen

Nanjing Medical University

Yangyang Song

Cangzhou Central Hospital

Xinyu Ke

National University Cancer Institute, Singapore

Vanessa Hui En Ng

National University Cancer Institute, Singapore

Wei Peng Yong

National University Cancer Institute, Singapore

Patrick Tan

Duke-NUS Medical School

Fernando Bellido Molias

National University Cancer Institute, Singapore

Raghav Sundar

National University of Singapore

Jimmy Bok Yan So

National University Hospital

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National University of Singapore

237

National University Cancer Institute, Singapore

168

Agency for Science, Technology and Research

National University Health System

National University Hospital

Institute of Molecular and Cell Biology

Duke-NUS Medical School

Nanyang Technological University

Genome Institute of Singapore

National Cancer Centre Singapore

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Supplementary Figure 1 from “3G” Trial: An RNA Editing Signature to Guide Gastric Cancer Chemotherapy

Ömer An Yangyang Song Xinyu Ke Jimmy Bok Yan So Raghav Sundar

Supplementary Figure 1

Signature (topology)

10.1158/0008-5472.22427002

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NCG 5.0: updates of a manually curated repository of cancer genes and associated properties from cancer mutational screenings

Nucleic Acids Research (2015)

Ömer An Giovanni Marco Dall’Olio Thanos P. Mourikis Francesca D. Ciccarelli

The Network of Cancer Genes (NCG, http://ncg.kcl.ac.uk/) is a manually curated repository of cancer genes derived from the scientific literature. Due to the increasing amount of cancer genomic data, we have introduced a more robust procedure to extract cancer genes from published cancer mutational screenings and two curators independently reviewed each publication. NCG release 5.0 (August 2015) collects 1571 cancer genes from 175 published studies that describe 188 mutational screenings of 13 315 cancer samples from 49 cancer types and 24 primary sites. In addition to collecting cancer genes, NCG also provides information on the experimental validation that supports the role of these genes in cancer and annotates their properties (duplicability, evolutionary origin, expression profile, function and interactions with proteins and miRNAs).

10.1093/nar/gkv1123

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Supplementary Table S8 from Antisense RNAs Influence Promoter Usage of Their Counterpart Sense Genes in Cancer

Fernando Bellido Molias Andre Sim Wai Yie Leong Ömer An Yangyang Song

List of 521 unique ncNATs expressed in non-tumor samples of one or multiple cancer/tissue types from TCGA and GTEx.

Table (database)

10.1158/0008-5472.22529123.v1

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Supplementary Table S3 from Antisense RNAs Influence Promoter Usage of Their Counterpart Sense Genes in Cancer

Fernando Bellido Molias Andre Sim Wai Yie Leong Ömer An Yangyang Song

List of ncNATs expressed in TCGA and GTEx non-tumor samples, for which their associated sense genes have two active alternative promoters

Table (database)

10.1158/0008-5472.22529126.v1

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Antisense RNAs Influence Promoter Usage of Their Counterpart Sense Genes in Cancer

Cancer Research (2021)

Fernando Bellido Molias Andre Sim Wai Yie Leong Ömer An Yangyang Song

Abstract Multiple noncoding natural antisense transcripts (ncNAT) are known to modulate key biological events such as cell growth or differentiation. However, the actual impact of ncNATs on cancer progression remains largely unknown. In this study, we identified a complete list of differentially expressed ncNATs in hepatocellular carcinoma. Among them, a previously undescribed ncNAT HNF4A-AS1L suppressed cancer cell growth by regulating its sense gene HNF4A, a well-known cancer driver, through a promoter-specific mechanism. HNF4A-AS1L selectively activated the HNF4A P1 promoter via HNF1A, which upregulated expression of tumor suppressor P1-driven isoforms, while having no effect on the oncogenic P2 promoter. RNA-seq data from 23 tissue and cancer types identified approximately 100 ncNATs whose expression correlated specifically with the activity of one promoter of their associated sense gene. Silencing of two of these ncNATs ENSG00000259357 and ENSG00000255031 (antisense to CERS2 and CHKA, respectively) altered the promoter usage of CERS2 and CHKA. Altogether, these results demonstrate that promoter-specific regulation is a mechanism used by ncNATs for context-specific control of alternative isoform expression of their counterpart sense genes. Significance: This study characterizes a previously unexplored role of ncNATs in regulation of isoform expression of associated sense genes, highlighting a mechanism of alternative promoter usage in cancer.

10.1158/0008-5472.can-21-1859

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Impact of CD151 overexpression on prognosis and therapy in non‐small cell lung cancer patients lacking EGFR mutations

Cell Proliferation (2024)

Amanda Huee‐Ping Wong Min En Nga Chin Yein Chin Yee Kit Tai Hung Chew Wong

This study investigates CD151, a protein linked to cancer progression, in non-small cell lung cancer (NSCLC) patients without epidermal growth factor receptor (EGFR) mutations. These patients often have limited treatment options. The study used retrospective analysis to examine 157 adenocarcinoma biopsy specimens and 199 patient cases from The Cancer Genome Atlas, correlating CD151 expression with patient survival. Cellular studies revealed that CD151 interacts with EGFR, influencing epidermal growth factor (EGF)-induced cell proliferation and the effectiveness of the EGFR inhibitor, erlotinib. A strong association was found between CD151 expression and EGFR mutation status. High CD151 expression in the absence of EGFR mutations is correlated with poorer survival outcomes. Biological assays showed that CD151 colocalizes and associates with EGFR, playing a crucial role in regulating EGF-induced cell proliferation via the AKT and ERK1/2 pathways. Importantly, CD151 expression was found to influence the anti-proliferative effects of the EGFR tyrosine kinase inhibitor, erlotinib. High CD151 expression, in the absence of EGFR mutations, was associated with poorer survival outcomes. It could serve as a potential prognostic marker and influence cellular responses to EGFR-targeted treatments. This study highlights CD151 as a potential novel target for therapeutic intervention in NSCLC, especially in populations lacking EGFR mutations.

Targeted Therapy

Erlotinib Hydrochloride

10.1111/cpr.13708

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Supplementary Figure 3 from “3G” Trial: An RNA Editing Signature to Guide Gastric Cancer Chemotherapy

Ömer An Yangyang Song Xinyu Ke Jimmy Bok Yan So Raghav Sundar

Supplementary Figure 3

Signature (topology)

10.1158/0008-5472.22426996

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Supplementary Figure 5 from “3G” Trial: An RNA Editing Signature to Guide Gastric Cancer Chemotherapy

Ömer An Yangyang Song Xinyu Ke Jimmy Bok Yan So Raghav Sundar

Supplementary Figure 5

Signature (topology)

10.1158/0008-5472.22426990.v1

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Database update NCG 4.0: the network of cancer genes in the era of massive mutational screenings of cancer genomes

Ömer An Vera Pendino Emanuele Ratti Marco Gentilini Francesca D. Ciccarelli

Division ofCancer Studies, King’s College London, London SE1 1UL, UK*Corresponding author: Tel: +44 (0)20 7848 6616; Fax: +44 (0)20 7848 6220; Email: francesca.ciccarelli@kcl.ac.ukSubmitted 29 November 2013; Revised 10 January 2014; Accepted 2 February 2014Citation details: An,O., Pendino,V., D’Antonio,M., et al. NCG 4.0: the network of cancer genes in the era of massive mutational screenings of cancergenomes. Database (2014) Vol. 2014: article ID bau015; doi:10.1093/database/bau015.

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FEZ1 participates in human embryonic brain development by modulating neuronal progenitor subpopulation specification and migration

bioRxiv (Cold Spring Harbor Laboratory) (2022)

Yinghua Qu Ömer An Henry Yang Yi‐Chin Toh John Jia En Chua

Abstract Abnormal neuronal networks arising from perturbations during early brain development contribute to neurodevelopmental disorders. Mutations and deletions of human Fasciculation and Elongation Protein Zeta 1 ( FEZ1 ) are found in schizophrenia and Jacobsen syndrome patients. However, its roles in human brain development and manifestation of clinical pathological symptoms remain unknown. Here, using human cerebral organoids (hCOs), we observed that FEZ1 expression is turned on early during brain development and is detectable in both neuroprogenitor subtypes and immature neurons. Deletion of FEZ1 disrupts expression of genes involved in neuronal and synaptic development. Using single-cell RNA sequencing, we further uncovered an abnormal expansion of homeodomain-only protein homeobox (HOPX) − outer radial glia (oRG) in FEZ1-null hCOs, occurring at the expense of HOPX + oRG. HOPX − oRGs show higher cell mobility as compared to HOPX + oRGs, which is accompanied by the ectopic localization of the neuroprogenitors to the outer layer of FEZ1-null hCOs. Moreover, abnormal encroachment of TBR2 + intermediate progenitors into CTIP2 + deep layer neurons indicated that cortical layer formation is disrupted in FEZ1-null hCOs. Collectively, our findings highlight the involvement of FEZ1 in early cortical brain development and how it contributes to neurodevelopmental disorders.

Progenitor

Ectopic expression

10.1101/2022.07.11.499073

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