ArticleCancer discovery2013
Systematic interrogation of 3q26 identifies TLOC1 and SKIL as cancer drivers.
Article in Cancer discovery, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
51 citing papers in PubMed, 1 synthesis or guideline pooled it, 77 citations in OpenAlex.
- Selective autophagy of intracellular organelles: recent research advances.Theranostics · 2021Pooled it
- Mechanotransduction-Induced Gene Expression Reveals Activation of TGFβ/SKIL/TAZ Axis and Supports Invasive Phenotype in Triple-Negative Breast Cancer.International journal of molecular sciences · 2026Article
- Article
- MECOM Locus classical transcript isoforms affect tumor immune microenvironment and different targets in ovarian cancer.Journal of ovarian research · 2024Article
- PLD1 is a key player in cancer stemness and chemoresistance: Therapeutic targeting of cross-talk between the PI3K/Akt and Wnt/β-catenin pathways.Experimental & molecular medicine · 2024Review
- E2F1 promotes cell migration in hepatocellular carcinoma via FNDC3B.FEBS open bio · 2024Article
- NSUN2 promotes colorectal cancer progression by enhancing SKIL mRNA stabilization.Clinical and translational medicine · 2024Article
- The 3q OncogeneInternational journal of molecular sciences · 2023Article
- Article
- Signaling pathways and targeted therapies in lung squamous cell carcinoma: mechanisms and clinical trials.Signal transduction and targeted therapy · 2022Review
- Sec62 promotes gastric cancer metastasis through mediating UPR-induced autophagy activation.Cellular and molecular life sciences : CMLS · 2022Article
- Effect of the 3q26-coding oncogeneFrontiers in physiology · 2022Article
- The endoplasmic reticulum membrane protein Sec62 as potential therapeutic target inFrontiers in physiology · 2022Review
- Antagonizing Sec62 function in intracellular CaFrontiers in physiology · 2022Article
- TNIK Is a Therapeutic Target in Lung Squamous Cell Carcinoma and Regulates FAK Activation through Merlin.Cancer discovery · 2021Article
- Complexity and Specificity of Sec61-Channelopathies: Human Diseases Affecting Gating of the Sec61 Complex.Cells · 2021Review
- Sec62 promotes stemness and chemoresistance of human colorectal cancer through activating Wnt/β-catenin pathway.Journal of experimental & clinical cancer research : CR · 2021Article
- Expression ofCancers · 2021Article
- New Therapeutic Opportunities for the Treatment of Squamous Cell Carcinomas: A Focus on Novel Driver Kinases.International journal of molecular sciences · 2021Review
- Identifying Key Somatic Copy Number Alterations Driving Dysregulation of Cancer Hallmarks in Lower-Grade Glioma.Frontiers in genetics · 2021Article
Corrections and comments
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Authors and funding
21 authors at 5 institutions in 1 country.
Funding
Abstract
unlabelled3q26 is frequently amplified in several cancer types with a common amplified region containing 20 genes. To identify cancer driver genes in this region, we interrogated the function of each of these genes by loss- and gain-of-function genetic screens. Specifically, we found that TLOC1 (SEC62) was selectively required for the proliferation of cell lines with 3q26 amplification. Increased TLOC1 expression induced anchorage-independent growth, and a second 3q26 gene, SKIL (SNON), facilitated cell invasion in immortalized human mammary epithelial cells. Expression of both TLOC1 and SKIL induced subcutaneous tumor growth. Proteomic studies showed that TLOC1 binds to DDX3X, which is essential for TLOC1-induced transformation and affected protein translation. SKIL induced invasion through upregulation of SLUG (SNAI2) expression. Together, these studies identify TLOC1 and SKIL as driver genes at 3q26 and more broadly suggest that cooperating genes may be coamplified in other regions with somatic copy number gain. SIGNIFICANCE: These studies identify TLOC1 and SKIL as driver genes in 3q26. These observations provide evidence that regions of somatic copy number gain may harbor cooperating genes of different but complementary functions.
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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 OpenQuestion graph.