ArticleOncogene2020
Integrative analysis of genomic amplification-dependent expression and loss-of-function screen identifies ASAP1 as a driver gene in triple-negative breast cancer progression.
Article in Oncogene, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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Who cites it
23 citing papers in PubMed, 43 citations in OpenAlex.
- Article
- Chaperonin proteins CCT5 and CCT7 epigenetically restrict the transition from pluripotency to totipotency in embryonic stem cells.Stem cell reports · 2026Article
- Multi-omics profiling uncovers immune-molecular clusters with distinct chemo-immunotherapeutic vulnerabilities in a mouse model of triple-negative breast cancer.Molecular cancer · 2026Article
- The oncogenic role of NSUN2 in lung adenocarcinoma by stabilizing CCT5 mRNA via a YBX1-dependent m5C modification.Molecular and cellular biochemistry · 2026Article
- CCT5 as a candidate biomarker in bladder cancer: functional validation and mechanistic clues.American journal of cancer research · 2026Article
- Centromere Protein F in Tumor Biology: Cancer's Achilles Heel.Cancer medicine · 2025Review
- ASAP1 and ARF1 Regulate Myogenic Differentiation in Rhabdomyosarcoma by Modulating TAZ Activity.Molecular cancer research : MCR · 2025Article
- Development and validation of a machine learning-driven mitochondrial gene signature for the diagnosis of breast cancer.Frontiers in immunology · 2025Article
- Role of ADP ribosylation factor guanylate kinase 1 in the malignant biological behavior of gastric cancer.Heliyon · 2024Article
- SPOP point mutations regulate substrate preference and affect its function.Cell death & disease · 2024Article
- Novel biomarkers to predict treatment response and prognosis in locally advanced rectal cancer undergoing neoadjuvant chemoradiotherapy.BMC cancer · 2023Article
- ASAP1 Expression in Invasive Breast Cancer and Its Prognostic Role.International journal of molecular sciences · 2023Article
- BICC1 drives pancreatic cancer progression by inducing VEGF-independent angiogenesis.Signal transduction and targeted therapy · 2023Article
- ASAP1 activates the IQGAP1/CDC42 pathway to promote tumor progression and chemotherapy resistance in gastric cancer.Cell death & disease · 2023Article
- Mitochondrial DNA methylation is a predictor of immunotherapy response and prognosis in breast cancer: scRNA-seq and bulk-seq data insights.Frontiers in immunology · 2023Article
- Nanomaterial-assisted CRISPR gene-engineering - A hallmark for triple-negative breast cancer therapeutics advancement.Materials today. Bio · 2022Review
- HiC1Dmetrics: framework to extract various one-dimensional features from chromosome structure data.Briefings in bioinformatics · 2022Article
- Correlation between Ferroptosis-Related Gene Signature and Immune Landscape, Prognosis in Breast Cancer.Journal of immunology research · 2022Article
- Clinicopathological Implications of ASAP1 Expression in Hepatocellular Carcinoma.Pathology oncology research : POR · 2022Article
- Inhibition of mutant KRAS-driven overexpression of ARF6 and MYC by an eIF4A inhibitor drug improves the effects of anti-PD-1 immunotherapy for pancreatic cancer.Cell communication and signaling : CCS · 2021Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The genetically heterogeneous triple-negative breast cancer (TNBC) continues to be an intractable disease, due to lack of effective targeted therapies. Gene amplification is a major event in tumorigenesis. Genes with amplification-dependent expression are being explored as therapeutic targets for cancer treatment. In this study, we have applied Analytical Multi-scale Identification of Recurring Events analysis and transcript quantification in the TNBC genome across 222 TNBC tumors and identified 138 candidate genes with positive correlation in copy number gain (CNG) and gene expression. siRNA-based loss-of-function screen of the candidate genes has validated EGFR, MYC, ASAP1, IRF2BP2, and CCT5 genes as drivers promoting proliferation in different TNBC cells. MYC, ASAP1, IRF2BP2, and CCT5 display frequent CNG and concurrent expression over 2173 breast cancer tumors (cBioPortal dataset). More frequently are MYC and ASAP1 amplified in TNBC tumors (>30%, n = 320). In particular, high expression of ASAP1, the ADP-ribosylation factor GTPase-activating protein, is significantly related to poor metastatic relapse-free survival of TNBC patients (n = 257, bc-GenExMiner). Furthermore, we have revealed that silencing of ASAP1 modulates numerous cytokine and apoptosis signaling components, such as IL1B, TRAF1, AIFM2, and MAP3K11 that are clinically relevant to survival outcomes of TNBC patients. ASAP1 has been reported to promote invasion and metastasis in various cancer cells. Our findings that ASAP1 is an amplification-dependent TNBC driver gene promoting TNBC cell proliferation, functioning upstream apoptosis components, and correlating to clinical outcomes of TNBC patients, support ASAP1 as a potential actionable target for TNBC treatment.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.