ArticleOncotarget2017
Decreased TOB1 expression and increased phosphorylation of nuclear TOB1 promotes gastric cancer.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 23 citations in OpenAlex.
- Reprogramming of hsa_circ_0008719 and its target miR-3615 induced by TOB1 in exosomes of gastric cancer cells: a contribution to inhibit gastric cancer progression.Scientific reports · 2025Article
- Cytoplasmic mRNA decay and quality control machineries in eukaryotes.Nature reviews. Genetics · 2025Review
- TOB1 inhibits the gastric cancer progression by focal adhesion pathway and ERK pathway based on transcriptional and metabolic sequencing.BMC cancer · 2024Article
- TOB1 modulates neutrophil phenotypes to influence gastric cancer progression and immunotherapy efficacy.Frontiers in immunology · 2024Article
- Methylation Mediated Downregulation of TOB1-AS1 and TOB1 Correlates with Malignant Progression and Poor Prognosis of Esophageal Squamous Cell Carcinoma.Digestive diseases and sciences · 2023Article
- Article
- The Overexpression of TOB1 Induces Autophagy in Gastric Cancer Cells by Secreting Exosomes.Disease markers · 2022Article
- Article
- Key Regulatory Differentially Expressed Genes in the Blood of Atrial Septal Defect Children Treated With Occlusion Devices.Frontiers in genetics · 2021Article
- TOB1 suppresses proliferation in K-Ras wild-type pancreatic cancer.Cancer medicine · 2020Article
- Nuclear ERK: Mechanism of Translocation, Substrates, and Role in Cancer.International journal of molecular sciences · 2019Review
- Phosphorylation of TOB1 at T172 and S320 is critical for gastric cancer proliferation and progression.American journal of translational research · 2019Article
- Association between the SNPs of theJournal of Cancer · 2018Article
Corrections and comments
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Authors and funding
17 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TOB1, a member of the BTG/TOB protein family, inhibits tumor cell proliferation. We previously observed down-regulation and phosphorylation of TOB1 in gastric cancer (GC). Here, we examined the subcellular distribution and clinical significance of TOB1 expression and phosphorylation in GC. Immunohistochemical analysis of 341 primary GC and corresponding normal gastric tissue samples demonstrated that nuclear TOB1 expression was lower in GC than normal tissue (80.4% vs. 92.4%), and decreased nuclear TOB1 expression correlated with high TNM stage. By contrast, phosphorylation of nuclear TOB1 was higher in GC than normal gastric tissue (66.0% vs. 36.4%), and was associated with poorly differentiated and high TNM stage tumors. Patients with intestinal type GC and increased nuclear TOB1 phosphorylation had poor overall survival. Multivariate survival analysis indicated the nuclear concentration of phosphorylated TOB1 was an independent prognostic factor for intestinal type GC. Overexpression of TOB1 containing mutations in its nuclear export signal inhibited GC cell proliferation, migration, and invasion compared to cells expressing TOB1 with the nuclear localization signal. Thus, decreased TOB1 expression and increased phosphorylation of nuclear TOB1 is associated with aggressive tumor behavior and poor prognosis in intestinal type GC. Additionally, TOB1 nuclear retention is critical for its anti-proliferative activity.
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