ArticlePeerJ2022
Involvement of TOB1 on autophagy in gastric cancer AGS cells
Article in PeerJ, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 9 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
- Association among Noncoding-RNAs, APRO Family Proteins, and Gut Microbiota in the Development of Breast Cancer.Oncology research · 2025Review
- TOB1 modulates neutrophil phenotypes to influence gastric cancer progression and immunotherapy efficacy.Frontiers in immunology · 2024Article
- A pan-cancer analysis of anti-proliferative protein family genes for therapeutic targets in cancer.Scientific reports · 2023Article
- Article
- The Overexpression of TOB1 Induces Autophagy in Gastric Cancer Cells by Secreting Exosomes.Disease markers · 2022Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundWe previously identified the tumor suppressor gene
methodsWestern blotting was used to detect the protein levels of TOB1, LC3, AKT, mTOR, phosphorylated (p) AKT, and p-mTOR. A double fluorescent GFP-RFP-LC3 fusion protein was used to trace autophagy by laser confocal microscopy. Autophagosomes were observed by transmission electron microscopy.
resultsThe conversion of LC3-I to LC3-II and the LC3-II/LC3-I ratio were significantly increased in AGS cells overexpressing TOB1 compared with control cells. Fluorescence imaging showed LC3 puncta at 48 h, and these puncta increased significantly at 72 h after TOB1 transfection compared with control tumor cells. The presence of autophagosomes in AGS cells was observed at 72 h after TOB1 transfection by transmission electron microscopy, and no autophagosomes were found in the control cells. Moreover, the levels of p-AKT and p -mTOR were lower in AGS cells than in control cancer cells.
conclusionOur results provide novel insight that TOB1 might suppress gastric cancer by inducing autophagy, possibly through decreasing phosphorylation and the subsequent activation of the AKT/mTOR signaling pathway.
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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.