ArticleInternational journal of biological sciences2014
SAMD9L inactivation promotes cell proliferation via facilitating G1-S transition in hepatitis B virus-associated hepatocellular carcinoma.
Article in International journal of biological sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- From a novel pathogenic SAMD9L variant to cohort-wide insights: Whole-genome sequencing highlights somatic genetic rescue and phenotypic heterogeneity.British journal of haematology · 2026Article
- A Novel Affordable and Reliable Framework for Accurate Detection and Comprehensive Analysis of Somatic Mutations in Cancer.International journal of molecular sciences · 2024Article
- Type I interferon pathway in pediatric systemic lupus erythematosus.World journal of pediatrics : WJP · 2024Review
- Functional Study of SAMD9L in Familial Gastric Cancer.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2023Article
- Integrated Analysis Identifies Upregulated SAMD9L as a Potential Biomarker Correlating with the Severity of Primary Sjögren's Syndrome.Journal of inflammation research · 2023Article
- Article
- Diagnosis and staging of HCV associated fibrosis, cirrhosis and hepatocellular carcinoma with target identification for miR-650, 552-3p, 676-3p, 512-5p and 147b.Cancer biomarkers : section A of Disease markers · 2022Article
- SAMD9L autoinflammatory or ataxia pancytopenia disease mutations activate cell-autonomous translational repression.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Germline SAMD9L truncation variants trigger global translational repression.The Journal of experimental medicine · 2021Article
- Identification of SAMD9L as a susceptibility locus for intravenous immunoglobulin resistance in Kawasaki disease by genome-wide association analysis.The pharmacogenomics journal · 2020Article
- In situ self-assembling Au-DNA complexes for targeted cancer bioimaging and inhibition.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Five-long non-coding RNA risk score system for the effective prediction of gastric cancer patient survival.Oncology letters · 2019Article
- Notch3-dependent β-catenin signaling mediates EGFR TKI drug persistence in EGFR mutant NSCLC.Nature communications · 2018Article
- CompoundExperimental and therapeutic medicine · 2018Article
- Whole Exome Sequencing Uncovers Germline Variants of Cancer-Related Genes in Sporadic Pheochromocytoma.International journal of genomics · 2018Article
- Ataxia-pancytopenia syndrome withNeurology. Genetics · 2017Article
- Gain-of-functionBlood · 2017Article
- Ataxia-Pancytopenia Syndrome Is Caused by Missense Mutations in SAMD9L.American journal of human genetics · 2016Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocellular carcinoma (HCC) is a highly malignant cancer with poor prognosis, and driver genes harboring genetic lesions and/or expression dysregulation contribute to hepatocarcinogenesis. Sterile Alpha Motif Domain-containing 9-like (SAMD9L) was a novel identified mutated gene in our previous study on exome sequencing of hepatitis B virus (HBV)-associated HCC, but its expression and role in HCC remain unknown. Here, we demonstrated that SAMD9L was frequently inactivated by somatic mutations, and that its expression was deregulated in HCC patients with hepatitis B virus (HBV) infection. SAMD9L knockdown significantly promoted cell proliferation, colony formation of SK-hep-1, QGY-7701, BEL-7721 and MHCC-97H HCC cells. Furthermore, SK-hep-1 and MHCC-97H cells with stable SAMD9L knockdown exhibited enhanced tumorigenicity in athymic mice. Interestingly, SAMD9L silence facilitated G1-S transition of cell cycle progression and led to the elevated activity of Wnt/β-catenin pathway. Collectively, these findings highlight a novel tumor-suppressive role of SAMD9L inactivation by somatic mutation and decreased expression in human HBV-related HCC.
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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.