ArticleOncology letters2017
Tumor necrosis factor receptor 2 promotes growth of colorectal cancer via the PI3K/AKT signaling pathway.
Article in Oncology letters, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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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
23 citing papers in PubMed, 39 citations in OpenAlex.
- Senolytic agent ABT-263 mitigates low- and high-LET radiation-induced gastrointestinal cancer development inAging · 2025Article
- Targeting TNFR2 for cancer immunotherapy: recent advances and future directions.Journal of translational medicine · 2024Review
- Altered expression of cytokines, chemokines, growth factors, and soluble receptors in patients with colorectal cancer, and correlation with treatment outcome.Cancer immunology, immunotherapy : CII · 2024Article
- Article
- Anti-TNFR2 Antibody-Conjugated PLGA Nanoparticles for Targeted Delivery of Adriamycin in Mouse Colon Cancer.Research (Washington, D.C.) · 2024Article
- TNFR2 promotes pancreatic cancer proliferation, migration, and invasion via the NF-κB signaling pathway.Aging · 2023Article
- Injured Endothelial Cell: A Risk Factor for Pulmonary Fibrosis.International journal of molecular sciences · 2023Review
- The Immunosuppressive Effect of TNFR2 Expression in the Colorectal Cancer Microenvironment.Biomedicines · 2023Review
- TNFR2 deficiency impairs the growth of mouse colon cancer.International journal of biological sciences · 2023Article
- Review
- Review
- Combination cancer immunotherapy targeting TNFR2 and PD-1/PD-L1 signaling reduces immunosuppressive effects in the microenvironment of pancreatic tumors.Journal for immunotherapy of cancer · 2022Article
- Deciphering the involvement of iron targets in colorectal cancer: a network biology approach.American journal of translational research · 2022Article
- Anti-Tumor Necrosis Factor Receptor 2 Antibody Combined With Anti-PD-L1 Therapy Exerts Robust Antitumor Effects in Breast Cancer.Frontiers in cell and developmental biology · 2021Article
- TNFR2: Role in Cancer Immunology and Immunotherapy.ImmunoTargets and therapy · 2021Review
- Up-regulation of tumor necrosis factor-α pathway survival genes and of the receptor TNFR2 in gastric cancer.World journal of gastrointestinal oncology · 2019Article
- Unraveling the Cellular Mechanism of Assembling Cholesterols for Selective Cancer Cell Death.Molecular cancer research : MCR · 2019Article
- The role and molecular mechanism of Trop2 induced epithelial-mesenchymal transition through mediated β-catenin in gastric cancer.Cancer medicine · 2019Article
- Advances in Tumor-Stroma Interactions: Emerging Role of Cytokine Network in Colorectal and Pancreatic Cancer.Journal of oncology · 2019Review
- Mesenchymal TNFR2 promotes the development of polyarthritis and comorbid heart valve stenosis.JCI insight · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor necrosis factor receptor 2 (TNFR2) is the receptor for tumor necrosis factor α (TNF-α). TNFR2 differs from tumor necrosis factor 1 (TNFR1) in various ways and is mainly expressed in hematopoietic and endothelial cells. However, studies about its functions in tumors are limited. The contributions of TNFR2 in colorectal cancer (CRC) remain unknown. In the present study, it was found that TNFR2 was positively associated with Ki67 expression in CRC tissues using immunohistochemistry (IHC), and western blot analysis found that Ki67 was upregulated by overexpressing TNFR2 in SW1116 cells and inhibited by silencing TNFR2 in HT29 cells. Methyl thiazolyl tetrazolium assay found that growth of SW1116 cells overexpressing TNFR2 was significantly increased compared with the control group and that the growth of HT29 cells subsequent to silencing TNFR2 was significantly decreased compared with the control group. Clone formation assay found that more clones were formed in SW1116 cells overexpressing TNFR2 than the control group, and less clones formed in HT29 cells subsequent to silencing TNFR2 than the control group. In addition, western blot analysis found that phosphorylation of protein kinase B (AKT) was activated subsequent to overexpressing TNFR2 in SW1116 cells, and inhibited following silencing of TNFR2 in HT29 cells. Additionally, treatment using LY294002 significantly abrogated the promotion of Ki67 expression, growth and clone formation abilities induced by TNFR2 overexpression in SW1116 cells. All the results suggest that TNFR2 can significantly promote CRC growth via the phosphoinositide 3-kinase/AKT signaling pathway; this provides evidential support for taking TNFR2 as a new target for CRC treatment.
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