ArticleProceedings of the National Academy of Sciences of the United States of America2015
Genomic alterations in BCL2L1 and DLC1 contribute to drug sensitivity in gastric cancer.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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39 citing papers in PubMed, 73 citations in OpenAlex.
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- Anti-apoptotic BCL-2 family proteins: from regulatory networks to therapeutic targeting.Oncogenesis · 2026Review
- Integrated Analysis of lncRNA-miRNA-mRNA ceRNA Network and Identification of Hub lncRNAs in Molecular Subtypes of Gastric Cancer as Potential Prognostic Indicators.Bioinformatics and biology insights · 2026Article
- Both direct and indirect suppression of MCL1 synergizes with BCLXL inhibition in preclinical models of gastric cancer.Cell death & disease · 2025Article
- RNA NAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Mutational signatures in 175 Chinese gastric cancer patients.BMC cancer · 2024Article
- A comprehensive benchmarking of machine learning algorithms and dimensionality reduction methods for drug sensitivity prediction.Briefings in bioinformatics · 2024Article
- Genome-wide CRISPR screen reveals the synthetic lethality between BCL2L1 inhibition and radiotherapy.Life science alliance · 2024Article
- Exploring the mechanism of ellagic acid against gastric cancer based on bioinformatics analysis and network pharmacology.Journal of cellular and molecular medicine · 2023Article
- Anti-apoptotic protein BCL-XL as a therapeutic vulnerability in gastric cancer.Animal models and experimental medicine · 2023Article
- DLC1 as Druggable Target for Specific Subsets of Gastric Cancer: An RNA-seq-Based Study.Medicina (Kaunas, Lithuania) · 2023Article
- Deregulation of apoptotic proteins by induction ofIranian journal of basic medical sciences · 2023Article
- Genomic features of Helicobacter pylori-naïve diffuse-type gastric cancer.The Journal of pathology · 2022Article
- Functional antagonism between CagA and DLC1 in gastric cancer.Cell death discovery · 2022Article
- CircZKSCAN1 Suppresses Hepatocellular Carcinoma Tumorigenesis by Regulating miR-873-5p/Downregulation of Deleted in Liver Cancer 1.Digestive diseases and sciences · 2021Article
- The circular RNA hsa_circ_000780 as a potential molecular diagnostic target for gastric cancer.BMC medical genomics · 2021Article
- A novel genomic classification system of gastric cancer via integrating multidimensional genomic characteristics.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2021Article
- A novel treatment strategy for lapatinib resistance in a subset of HER2-amplified gastric cancer.BMC cancer · 2021Article
- Transcript-Level Dysregulation ofCancers · 2021Article
- Oncogenic Role of miR-200c-3p in High-Grade Serous Ovarian Cancer Progression via Targeting the 3'-Untranslated Region of DLC1.International journal of environmental research and public health · 2021Article
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Authors and funding
21 authors at 2 institutions in 3 countries.
Funding
Abstract
Gastric cancer (GC) is the third leading cause of cancer-related deaths worldwide. Recent high-throughput analyses of genomic alterations revealed several driver genes and altered pathways in GC. However, therapeutic applications from genomic data are limited, largely as a result of the lack of druggable molecular targets and preclinical models for drug selection. To identify new therapeutic targets for GC, we performed array comparative genomic hybridization (aCGH) of DNA from 103 patients with GC for copy number alteration (CNA) analysis, and whole-exome sequencing from 55 GCs from the same patients for mutation profiling. Pathway analysis showed recurrent alterations in the Wnt signaling [APC, CTNNB1, and DLC1 (deleted in liver cancer 1)], ErbB signaling (ERBB2, PIK3CA, and KRAS), and p53 signaling/apoptosis [TP53 and BCL2L1 (BCL2-like 1)] pathways. In 18.4% of GC cases (19/103), amplification of the antiapoptotic gene BCL2L1 was observed, and subsequently a BCL2L1 inhibitor was shown to markedly decrease cell viability in BCL2L1-amplified cell lines and in similarly altered patient-derived GC xenografts, especially when combined with other chemotherapeutic agents. In 10.9% of cases (6/55), mutations in DLC1 were found and were also shown to confer a growth advantage for these cells via activation of Rho-ROCK signaling, rendering these cells more susceptible to a ROCK inhibitor. Taken together, our study implicates BCL2L1 and DLC1 as potential druggable targets for specific subsets of GC cases.
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