ArticleBioengineered2022
Transcriptional activation of Proteasome 26S non-ATPase subunit 7 by forkhead box P3 participates in gastric cancer cell proliferation and apoptosis.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- [Research and Therapeutic Advances of 26S Proteasome Subunit in Non-small Cell Lung Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2025Review
- Deubiquitinase PSMD7 facilitates pancreatic cancer progression through activating Nocth1 pathway via modifying SOX2 degradation.Cell & bioscience · 2024Article
- Advances in Foxp3+ regulatory T cells (Foxp3+ Treg) and key factors in digestive malignancies.Frontiers in immunology · 2024Review
- 19S Proteasome Subunits as Oncogenes and Prognostic Biomarkers in FLT3-Mutated Acute Myeloid Leukemia (AML).International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Proteasome 26S non-ATPase subunit 7 (PSMD7) and forkhead box P3 (FOXP3) have been found to be both upregulated in gastric cancer tissues. FOXP3 was also predicted to have binding sites on PSMD7 promoter. Thus, this study investigated the relationship between PSMD7 and FOXP3 and their roles in gastric cancer. Bioinformatic databases predicted PSMD7 expression in non-cancerous gastric tissue and gastric cancer tissue, as well as the correlation between PSMD7 and the overall/disease free survival. PSMD7 expression in non-cancerous gastric tissue or cells and gastric cancer tissue or cells was detected by qPCR and Western blot. After PSMD7 downregulation by siRNA interference, cell viability, colony-forming capacity and cell apoptosis were analyzed with cell counting kit-8 assay, colony formation assay and terminal deoxynucleotidyl transferasemediated dUTP nick end-labeling. Proliferation and apoptosis markers were assayed by qPCR and Western blot. Dual-luciferase reporter and chromatin immunoprecipitation assays were performed to look at the binding relationship between FOXP3 and PSMD7 promoter. Cell proliferation and apoptosis were examined again after co-transfection of PSMD7 siRNA plasmid and FOXP3 overexpression plasmid. PSMD7 expression was much higher in gastric cancer tissue and cell lines. Interference with PSMD7 decreased gastric cancer cell viability, inhibited their proliferation and colony formation and promoted cell apoptosis. FOXP3 was found to bind to PSMD7 promoter and activate PSMD7 expression. Overexpression of FOXP3 could rescue the effects of PSMD7 knockdown on gastric cancer cells. PSMD7 is involved in the proliferation and apoptosis of gastric cancer cells and can be transcriptionally regulated by FOXP3.
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Registered trials
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